PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 33915156-0 2021 A protein-fragment complementation assay reveals that celastrol and gambogic acid suppress ERalpha mutants in breast cancer. celastrol 54-63 estrogen receptor 1 Homo sapiens 91-98 33915156-6 2021 We then collected and screened a natural product library for potential ERalpha antagonists via GLPCA and identified celastrol and gambogic acid as new antagonists of the ERalpha Y537S mutant. celastrol 116-125 estrogen receptor 1 Homo sapiens 170-177 33915156-8 2021 Importantly, we further demonstrated that celastrol and gambogic acid exhibit synergistic antiproliferative and pro-apoptotic effects when combined with an approved CDK4/6 inhibitor abemaciclib in breast cancer cells expressing ERalpha Y537S. celastrol 42-51 cyclin dependent kinase 4 Homo sapiens 165-171 33915156-8 2021 Importantly, we further demonstrated that celastrol and gambogic acid exhibit synergistic antiproliferative and pro-apoptotic effects when combined with an approved CDK4/6 inhibitor abemaciclib in breast cancer cells expressing ERalpha Y537S. celastrol 42-51 estrogen receptor 1 Homo sapiens 228-235 33965112-0 2021 Improved delivery system for celastrol-loaded magnetic Fe3O4/alpha-Fe2O3 heterogeneous nanorods: HIF-1alpha-related apoptotic effects on SMMC-7721 cell. celastrol 29-38 hypoxia inducible factor 1 subunit alpha Homo sapiens 97-107 33845380-0 2021 Discovery of novel celastrol-triazole derivatives with Hsp90-Cdc37 disruption to induce tumor cell apoptosis. celastrol 19-28 heat shock protein 90 alpha family class A member 1 Homo sapiens 55-60 33845380-0 2021 Discovery of novel celastrol-triazole derivatives with Hsp90-Cdc37 disruption to induce tumor cell apoptosis. celastrol 19-28 cell division cycle 37, HSP90 cochaperone Homo sapiens 61-66 33999692-8 2021 Celastrol treatment inhibited the production of both IL-23 and IL-17 in PBMCs of SO patients in a dose-dependent manner. celastrol 0-9 interleukin 23 subunit alpha Homo sapiens 53-58 34053427-10 2022 (4) Compared with the control group, the Celastrol treatment also reduced the expression of the mTOR signaling pathway related proteins, suggesting that the mTOR signaling pathway may be involved in the process of Celastrol inhibiting the proliferation of the SGC7901/DDP cells and reducing their drug resistance. celastrol 41-50 mechanistic target of rapamycin kinase Homo sapiens 96-100 34053427-10 2022 (4) Compared with the control group, the Celastrol treatment also reduced the expression of the mTOR signaling pathway related proteins, suggesting that the mTOR signaling pathway may be involved in the process of Celastrol inhibiting the proliferation of the SGC7901/DDP cells and reducing their drug resistance. celastrol 41-50 mechanistic target of rapamycin kinase Homo sapiens 157-161 34053427-10 2022 (4) Compared with the control group, the Celastrol treatment also reduced the expression of the mTOR signaling pathway related proteins, suggesting that the mTOR signaling pathway may be involved in the process of Celastrol inhibiting the proliferation of the SGC7901/DDP cells and reducing their drug resistance. celastrol 214-223 mechanistic target of rapamycin kinase Homo sapiens 96-100 34053427-10 2022 (4) Compared with the control group, the Celastrol treatment also reduced the expression of the mTOR signaling pathway related proteins, suggesting that the mTOR signaling pathway may be involved in the process of Celastrol inhibiting the proliferation of the SGC7901/DDP cells and reducing their drug resistance. celastrol 214-223 mechanistic target of rapamycin kinase Homo sapiens 157-161 34053427-11 2022 (5) Significantly, the combination of Celastrol and DDP reduced the expression of P-gp, MRP1, and BCRP in the SGC7901/DPP cells. celastrol 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 82-86 34053427-11 2022 (5) Significantly, the combination of Celastrol and DDP reduced the expression of P-gp, MRP1, and BCRP in the SGC7901/DPP cells. celastrol 38-47 ATP binding cassette subfamily C member 1 Homo sapiens 88-92 34053427-11 2022 (5) Significantly, the combination of Celastrol and DDP reduced the expression of P-gp, MRP1, and BCRP in the SGC7901/DPP cells. celastrol 38-47 BCR pseudogene 1 Homo sapiens 98-102 34053427-12 2022 CONCLUSION: Celastrol can inhibit the proliferation of the SGC7901/DDP cells, induce their apoptosis, and reduce the expression of drug resistance genes, probably by inhibiting the expression of the proteins related to the mTOR signaling pathway. celastrol 12-21 mechanistic target of rapamycin kinase Homo sapiens 223-227 33846813-0 2021 Celastrol attenuates the inflammatory response by inhibiting IL-1beta expression in triple-negative breast cancer cells. celastrol 0-9 interleukin 1 alpha Homo sapiens 61-69 33846813-2 2021 In the present study, the functional roles of IL-1beta (IL1B) and the inhibitory effect of celastrol on IL1B expression were investigated in triple-negative breast cancer (TNBC) cells. celastrol 91-100 interleukin 1 beta Homo sapiens 104-108 33846813-3 2021 The data revealed that celastrol markedly decreased IL1B expression and suppressed TNBC cell proliferation in a dose-dependent manner. celastrol 23-32 interleukin 1 beta Homo sapiens 52-56 33846813-7 2021 Celastrol also promoted IL1B downregulation through the suppression of the MEK/ERK-dependent pathway. celastrol 0-9 interleukin 1 beta Homo sapiens 24-28 33846813-7 2021 Celastrol also promoted IL1B downregulation through the suppression of the MEK/ERK-dependent pathway. celastrol 0-9 mitogen-activated protein kinase kinase 7 Homo sapiens 75-78 33846813-7 2021 Celastrol also promoted IL1B downregulation through the suppression of the MEK/ERK-dependent pathway. celastrol 0-9 mitogen-activated protein kinase 1 Homo sapiens 79-82 33846813-8 2021 Furthermore, the results also revealed a decrease in IL1B-induced IL8, MMP-1, and MMP-9 expression in response to celastrol treatment. celastrol 114-123 interleukin 1 beta Homo sapiens 53-57 33846813-8 2021 Furthermore, the results also revealed a decrease in IL1B-induced IL8, MMP-1, and MMP-9 expression in response to celastrol treatment. celastrol 114-123 C-X-C motif chemokine ligand 8 Homo sapiens 66-69 33846813-8 2021 Furthermore, the results also revealed a decrease in IL1B-induced IL8, MMP-1, and MMP-9 expression in response to celastrol treatment. celastrol 114-123 matrix metallopeptidase 1 Homo sapiens 71-76 33846813-8 2021 Furthermore, the results also revealed a decrease in IL1B-induced IL8, MMP-1, and MMP-9 expression in response to celastrol treatment. celastrol 114-123 matrix metallopeptidase 9 Homo sapiens 82-87 33846813-9 2021 The induction of cellular invasion by IL1B was also markedly decreased by celastrol. celastrol 74-83 interleukin 1 beta Homo sapiens 38-42 33846813-10 2021 Collectively, the present study results suggested celastrol as an effective drug for the treatment of TNBC, involving a reduction in IL1B expression, activity or signaling pathways. celastrol 50-59 interleukin 1 beta Homo sapiens 133-137 34053427-9 2022 However, after treating with Celastrol, the expression levels of P-gp, MRP1, and BCRP in the SGC7901/DPP cells were significantly reduced (P<0.05). celastrol 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 65-69 34053427-9 2022 However, after treating with Celastrol, the expression levels of P-gp, MRP1, and BCRP in the SGC7901/DPP cells were significantly reduced (P<0.05). celastrol 29-38 ATP binding cassette subfamily C member 1 Homo sapiens 71-75 34053427-9 2022 However, after treating with Celastrol, the expression levels of P-gp, MRP1, and BCRP in the SGC7901/DPP cells were significantly reduced (P<0.05). celastrol 29-38 BCR pseudogene 1 Homo sapiens 81-85 33999692-8 2021 Celastrol treatment inhibited the production of both IL-23 and IL-17 in PBMCs of SO patients in a dose-dependent manner. celastrol 0-9 interleukin 17A Homo sapiens 63-68 33999692-9 2021 In PBMCs isolated from SO patients and healthy controls, the administration of recombinant human IL-23 (rIL-23) enhanced the production of IL-17, which was then suppressed by co-stimulation with celastrol. celastrol 195-204 interleukin 23 subunit alpha Homo sapiens 97-102 33999692-9 2021 In PBMCs isolated from SO patients and healthy controls, the administration of recombinant human IL-23 (rIL-23) enhanced the production of IL-17, which was then suppressed by co-stimulation with celastrol. celastrol 195-204 interleukin 17A Homo sapiens 139-144 33999692-10 2021 Also, celastrol treatment reduced rIL-23-induced phosphorylation of STAT3 in PBMCs isolated from SO patients. celastrol 6-15 signal transducer and activator of transcription 3 Homo sapiens 68-73 33999692-11 2021 Conclusions: Celastrol can reduce the production of IL-17 in PBMCs of SO patients. celastrol 13-22 interleukin 17A Homo sapiens 52-57 33753246-4 2021 In reported studies, the anti-obesity effect of celastrol resulted from regulating leptin sensitivity, energy metabolism, inflammation, lipid metabolism and even gut microbiota. celastrol 48-57 leptin Homo sapiens 83-89 34000513-9 2021 RESULTS: Findings indicated that tripterine suppressed BC cells" viability, proliferation, migration, invasion capacity and Bcl-2 protein expression, but it induced BC cells" Bax protein expression. celastrol 33-43 BCL2 apoptosis regulator Homo sapiens 124-129 34000513-9 2021 RESULTS: Findings indicated that tripterine suppressed BC cells" viability, proliferation, migration, invasion capacity and Bcl-2 protein expression, but it induced BC cells" Bax protein expression. celastrol 33-43 BCL2 associated X, apoptosis regulator Homo sapiens 175-178 34000513-10 2021 It was also found miR-184 expression was high in the BC cell lines treated with tripterine and that miR-184 overexpression reduced the viability, proliferation, and invasion abilities of BC cells under tripterine treatment. celastrol 80-90 microRNA 184 Homo sapiens 18-25 34000513-10 2021 It was also found miR-184 expression was high in the BC cell lines treated with tripterine and that miR-184 overexpression reduced the viability, proliferation, and invasion abilities of BC cells under tripterine treatment. celastrol 202-212 microRNA 184 Homo sapiens 18-25 34000513-10 2021 It was also found miR-184 expression was high in the BC cell lines treated with tripterine and that miR-184 overexpression reduced the viability, proliferation, and invasion abilities of BC cells under tripterine treatment. celastrol 202-212 microRNA 184 Homo sapiens 100-107 34000513-11 2021 Interference with miR-184 neutralized the effects of tripterine on BC cell viability, proliferation and invasion. celastrol 53-63 microRNA 184 Homo sapiens 18-25 34000513-12 2021 CONCLUSION: This research suggested that by interacting with miR-184, tripterine could restrain the progression of BC. celastrol 70-80 microRNA 184 Homo sapiens 61-68 32176932-8 2021 RESULTS: The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1beta signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. celastrol 161-170 interferon activated gene 208 Mus musculus 221-246 32176932-8 2021 RESULTS: The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1beta signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. celastrol 161-170 NLR family, pyrin domain containing 3 Mus musculus 248-253 32176932-8 2021 RESULTS: The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1beta signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. celastrol 161-170 caspase 1 Mus musculus 255-264 32176932-8 2021 RESULTS: The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1beta signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. celastrol 161-170 interleukin 1 beta Mus musculus 265-282 32176932-8 2021 RESULTS: The results demonstrated that the effect of HFD on inflammatory cytokines in mice with apoE-/- background was reversed by celastrol administration, and celastrol treatment inhibited the NOD-like receptor family, pyrin domain containing 3 (NLRP3)/caspase-1/interleukin-1beta signaling cascades in peripheral blood mononuclear cells from HFD-fed apoE-/- mice. celastrol 161-170 apolipoprotein E Mus musculus 353-357 32176932-10 2021 Furthermore, celastrol inhibited the pro-thrombotic effects of HFD in apoE-/- mice, and the underlying mechanism was mediated, at least partially, through the suppression of matrix metalloproteinase-2 and -9 expression. celastrol 13-22 apolipoprotein E Mus musculus 70-74 32176932-10 2021 Furthermore, celastrol inhibited the pro-thrombotic effects of HFD in apoE-/- mice, and the underlying mechanism was mediated, at least partially, through the suppression of matrix metalloproteinase-2 and -9 expression. celastrol 13-22 matrix metallopeptidase 2 Mus musculus 174-207 32176932-11 2021 CONCLUSIONS: Celastrol administration significantly attenuated HFD-induced inflammatory reaction, platelet aggregation and thrombosis in apoE-/- mice, and celastrol may be used as a drug for the prevention of HFD-induced inflammatory reaction and thrombus. celastrol 13-22 apolipoprotein E Mus musculus 137-141 32176932-0 2021 Enhanced Inflammatory Reaction and Thrombosis in High-Fat Diet-Fed ApoE-/- Mice are Attenuated by Celastrol. celastrol 98-107 CD36 molecule Mus musculus 54-57 32176932-0 2021 Enhanced Inflammatory Reaction and Thrombosis in High-Fat Diet-Fed ApoE-/- Mice are Attenuated by Celastrol. celastrol 98-107 apolipoprotein E Mus musculus 67-71 33753246-5 2021 Celastrol reversed insulin resistance via multiple routes to protect against type 2 diabetes. celastrol 0-9 insulin Homo sapiens 19-26 33924995-0 2021 Celastrol and Triptolide Suppress Stemness in Triple Negative Breast Cancer: Notch as a Therapeutic Target for Stem Cells. celastrol 0-9 notch receptor 1 Homo sapiens 77-82 33904854-0 2021 Correction: Systematic identification of celastrol-binding proteins reveals that Shoc2 is inhibited by celastrol. celastrol 41-50 SHOC2 leucine rich repeat scaffold protein Homo sapiens 81-86 33904854-0 2021 Correction: Systematic identification of celastrol-binding proteins reveals that Shoc2 is inhibited by celastrol. celastrol 103-112 SHOC2 leucine rich repeat scaffold protein Homo sapiens 81-86 33924995-9 2021 Both celastrol or triptolide reduced Notch -1 activation and expression of its downstream target proteins HES-1 and HEY-1. celastrol 5-14 notch receptor 1 Homo sapiens 37-45 33924995-9 2021 Both celastrol or triptolide reduced Notch -1 activation and expression of its downstream target proteins HES-1 and HEY-1. celastrol 5-14 hes family bHLH transcription factor 1 Homo sapiens 106-111 33924995-9 2021 Both celastrol or triptolide reduced Notch -1 activation and expression of its downstream target proteins HES-1 and HEY-1. celastrol 5-14 hes related family bHLH transcription factor with YRPW motif 1 Homo sapiens 116-121 33870466-13 2021 Finally, mTOR was determined as the most likely therapeutic target of celastrol in OA. celastrol 70-79 mechanistic target of rapamycin kinase Homo sapiens 9-13 33930802-0 2021 Design, synthesis of novel celastrol derivatives and study on their antitumor growth through HIF-1alpha pathway. celastrol 27-36 hypoxia inducible factor 1, alpha subunit Mus musculus 93-103 33930802-1 2021 Four series of hypoxia-inducible factor-1 alpha (HIF-1alpha) functioning derivatives stemming from modifications to the C-29 carboxyl group of celastrol were designed and synthesized, and their anticancer activities were evaluated. celastrol 143-152 hypoxia inducible factor 1, alpha subunit Mus musculus 15-47 33930802-1 2021 Four series of hypoxia-inducible factor-1 alpha (HIF-1alpha) functioning derivatives stemming from modifications to the C-29 carboxyl group of celastrol were designed and synthesized, and their anticancer activities were evaluated. celastrol 143-152 hypoxia inducible factor 1, alpha subunit Mus musculus 49-59 33870466-16 2021 mTOR is the most likely therapeutic target of celastrol in OA. celastrol 46-55 mechanistic target of rapamycin kinase Homo sapiens 0-4 33675143-8 2021 Furthermore, co-treatment with erastin and celastrol initiated ATG5/ATG7-dependent autophagy, PINK1/Parkin-dependent mitophagy, as well as the expression of heat shock proteins (HSP) in an HSF1-dependent manner. celastrol 43-52 autophagy related 5 Homo sapiens 63-67 33935779-0 2021 Celastrol Attenuates Lipid Accumulation and Stemness of Clear Cell Renal Cell Carcinoma via CAV-1/LOX-1 Pathway. celastrol 0-9 caveolin 1 Homo sapiens 92-97 33935779-0 2021 Celastrol Attenuates Lipid Accumulation and Stemness of Clear Cell Renal Cell Carcinoma via CAV-1/LOX-1 Pathway. celastrol 0-9 oxidized low density lipoprotein receptor 1 Homo sapiens 98-103 33935779-8 2021 Celastrol reduced lipid accumulation and caveolae abundance, inhibited the binding of CAV-1 and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in ccRCC cells. celastrol 0-9 caveolin 1 Homo sapiens 86-91 33935779-8 2021 Celastrol reduced lipid accumulation and caveolae abundance, inhibited the binding of CAV-1 and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in ccRCC cells. celastrol 0-9 oxidized low density lipoprotein receptor 1 Homo sapiens 153-158 33935779-9 2021 Furthermore, celastrol attenuated stemness through blocking Wnt/beta-catenin pathway after knockdown of CAV-1 and LOX-1. celastrol 13-22 catenin beta 1 Homo sapiens 64-76 33935779-9 2021 Furthermore, celastrol attenuated stemness through blocking Wnt/beta-catenin pathway after knockdown of CAV-1 and LOX-1. celastrol 13-22 caveolin 1 Homo sapiens 104-109 33935779-9 2021 Furthermore, celastrol attenuated stemness through blocking Wnt/beta-catenin pathway after knockdown of CAV-1 and LOX-1. celastrol 13-22 oxidized low density lipoprotein receptor 1 Homo sapiens 114-119 33675143-8 2021 Furthermore, co-treatment with erastin and celastrol initiated ATG5/ATG7-dependent autophagy, PINK1/Parkin-dependent mitophagy, as well as the expression of heat shock proteins (HSP) in an HSF1-dependent manner. celastrol 43-52 autophagy related 7 Homo sapiens 68-72 33675143-8 2021 Furthermore, co-treatment with erastin and celastrol initiated ATG5/ATG7-dependent autophagy, PINK1/Parkin-dependent mitophagy, as well as the expression of heat shock proteins (HSP) in an HSF1-dependent manner. celastrol 43-52 PTEN induced kinase 1 Homo sapiens 94-99 33675143-8 2021 Furthermore, co-treatment with erastin and celastrol initiated ATG5/ATG7-dependent autophagy, PINK1/Parkin-dependent mitophagy, as well as the expression of heat shock proteins (HSP) in an HSF1-dependent manner. celastrol 43-52 heat shock transcription factor 1 Homo sapiens 189-193 33472404-0 2021 Identification of Celastrol As a Novel Therapeutic Agent for Pulmonary Arterial Hypertension and Right Ventricular Failure Through Suppression of Bsg (Basigin)/CyPA (Cyclophilin A). celastrol 18-27 basigin Mus musculus 146-149 33472404-0 2021 Identification of Celastrol As a Novel Therapeutic Agent for Pulmonary Arterial Hypertension and Right Ventricular Failure Through Suppression of Bsg (Basigin)/CyPA (Cyclophilin A). celastrol 18-27 basigin Mus musculus 151-158 33472404-0 2021 Identification of Celastrol As a Novel Therapeutic Agent for Pulmonary Arterial Hypertension and Right Ventricular Failure Through Suppression of Bsg (Basigin)/CyPA (Cyclophilin A). celastrol 18-27 peptidylprolyl isomerase A Mus musculus 160-164 33472404-0 2021 Identification of Celastrol As a Novel Therapeutic Agent for Pulmonary Arterial Hypertension and Right Ventricular Failure Through Suppression of Bsg (Basigin)/CyPA (Cyclophilin A). celastrol 18-27 peptidylprolyl isomerase A Mus musculus 166-179 33472404-8 2021 Treatment with celastrol, which we identified as a suppressor of Bsg and CyPA by drug screening, decreased proliferation, reactive oxygen species, and inflammatory cytokines in pulmonary artery smooth muscle cells. celastrol 15-24 basigin Mus musculus 65-68 33472404-8 2021 Treatment with celastrol, which we identified as a suppressor of Bsg and CyPA by drug screening, decreased proliferation, reactive oxygen species, and inflammatory cytokines in pulmonary artery smooth muscle cells. celastrol 15-24 peptidylprolyl isomerase A Mus musculus 73-77 33472404-9 2021 Furthermore, celastrol treatment ameliorated RV systolic pressure, hypertrophy, fibrosis, and dysfunction in hypoxia-induced PH in mice and SU5416/hypoxia-induced PH in rats with reduced Bsg, CyPA, and inflammatory cytokines in the hearts and lungs. celastrol 13-22 basigin (Ok blood group) Rattus norvegicus 187-190 33472404-9 2021 Furthermore, celastrol treatment ameliorated RV systolic pressure, hypertrophy, fibrosis, and dysfunction in hypoxia-induced PH in mice and SU5416/hypoxia-induced PH in rats with reduced Bsg, CyPA, and inflammatory cytokines in the hearts and lungs. celastrol 13-22 peptidylprolyl isomerase A Rattus norvegicus 192-196 33472404-10 2021 CONCLUSIONS: These results indicate that elevated Bsg in pressure-overloaded RV exacerbates RV dysfunction and that celastrol ameliorates RV dysfunction in PH model animals by suppressing Bsg and its ligand CyPA. celastrol 116-125 basigin (Ok blood group) Rattus norvegicus 188-191 33472404-10 2021 CONCLUSIONS: These results indicate that elevated Bsg in pressure-overloaded RV exacerbates RV dysfunction and that celastrol ameliorates RV dysfunction in PH model animals by suppressing Bsg and its ligand CyPA. celastrol 116-125 peptidylprolyl isomerase A Rattus norvegicus 207-211 33472404-11 2021 Thus, celastrol can be a novel drug for PH and RV failure that targets Bsg and CyPA. celastrol 6-15 basigin (Ok blood group) Rattus norvegicus 71-74 33472404-11 2021 Thus, celastrol can be a novel drug for PH and RV failure that targets Bsg and CyPA. celastrol 6-15 peptidylprolyl isomerase A Rattus norvegicus 79-83 33591981-7 2021 Finally, we found that drugs targeting the identified RB1 interacting genes/pathways, such as UNC3230, PYR-41, TAK-243, isoginkgetin, madrasin, and celastrol also elicit SL in human cancer cell lines. celastrol 148-157 RB transcriptional corepressor 1 Homo sapiens 54-57 33559709-0 2021 Tripterine ameliorates monosodium urate crystal-induced gouty arthritis by altering macrophage polarization via the miR-449a/NLRP3 axis. celastrol 0-10 microRNA 449a Mus musculus 116-124 33559709-0 2021 Tripterine ameliorates monosodium urate crystal-induced gouty arthritis by altering macrophage polarization via the miR-449a/NLRP3 axis. celastrol 0-10 NLR family, pyrin domain containing 3 Mus musculus 125-130 33574707-13 2021 Furthermore, celastrol exerted the anti-HCC effect in vitro through the miR-223-3p/CXCR4 axis. celastrol 13-22 microRNA 223 Homo sapiens 72-79 33574707-13 2021 Furthermore, celastrol exerted the anti-HCC effect in vitro through the miR-223-3p/CXCR4 axis. celastrol 13-22 C-X-C motif chemokine receptor 4 Homo sapiens 83-88 33106373-5 2021 The potential SHOC2 inhibitor celastrol phenocopied SHOC2 depletion. celastrol 30-39 SHOC2 leucine rich repeat scaffold protein Homo sapiens 14-19 33383300-0 2021 Celastrol nanoemulsion induces immunogenicity and downregulates PD-L1 to boost abscopal effect in melanoma therapy. celastrol 0-9 CD274 molecule Homo sapiens 64-69 33383300-3 2021 Herein, we show that celastrol (CEL) induced not only strong ICD but also downregulation of PD-L1 expression of tumor cells. celastrol 21-30 CD274 molecule Homo sapiens 92-97 33383300-3 2021 Herein, we show that celastrol (CEL) induced not only strong ICD but also downregulation of PD-L1 expression of tumor cells. celastrol 32-35 CD274 molecule Homo sapiens 92-97 33106373-5 2021 The potential SHOC2 inhibitor celastrol phenocopied SHOC2 depletion. celastrol 30-39 SHOC2 leucine rich repeat scaffold protein Homo sapiens 52-57 33641477-0 2021 EXPRESSION OF CONCERN: "Tripterine up-regulates miR-223 to alleviate lipopolysaccharides-induced damage in murine chondrogenic ATDC5 cells". celastrol 24-34 microRNA 223 Mus musculus 48-55 33554800-8 2021 Among which sVCAM-1 and sICAM-1 of leucocyte, NB4 cell, P-selectin and adhesion molecules in tripterine group showed significant difference as compared with arsenic trioxide group (P<0.05). celastrol 93-103 selectin P Homo sapiens 56-66 33387968-0 2021 Celastrol attenuates ischemia/reperfusion-mediated memory dysfunction by downregulating AK005401/MAP3K12. celastrol 0-9 mitogen-activated protein kinase kinase kinase 12 Mus musculus 97-104 33387968-10 2021 Celastrol increased antioxidant capacity, inhibited cell apoptosis, and improved mitochondrial function, effectively improving learning and memory by downregulating AK005401 and MAP3K12 and activating PI3K/Akt. celastrol 0-9 mitogen-activated protein kinase kinase kinase 12 Mus musculus 178-185 33387968-10 2021 Celastrol increased antioxidant capacity, inhibited cell apoptosis, and improved mitochondrial function, effectively improving learning and memory by downregulating AK005401 and MAP3K12 and activating PI3K/Akt. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 206-209 33387968-11 2021 CONCLUSIONS: The AK005401/MAP3K12 signaling pathway has an important role in I/R-mediated hippocampal injury, and celastrol can potentially reduce or possibly prevent I/R-induced neuronal injury by downregulating AK005401/MAP3K12 signaling. celastrol 114-123 mitogen-activated protein kinase kinase kinase 12 Mus musculus 26-33 33387968-11 2021 CONCLUSIONS: The AK005401/MAP3K12 signaling pathway has an important role in I/R-mediated hippocampal injury, and celastrol can potentially reduce or possibly prevent I/R-induced neuronal injury by downregulating AK005401/MAP3K12 signaling. celastrol 114-123 mitogen-activated protein kinase kinase kinase 12 Mus musculus 222-229 33255023-0 2021 Lactoferrin-dual drug nanoconjugate: Synergistic anti-tumor efficacy of docetaxel and the NF-kappaB inhibitor celastrol. celastrol 110-119 lactotransferrin Mus musculus 0-11 33255023-0 2021 Lactoferrin-dual drug nanoconjugate: Synergistic anti-tumor efficacy of docetaxel and the NF-kappaB inhibitor celastrol. celastrol 110-119 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 90-99 32776627-5 2021 Further studies found that celastrol decreased the infiltration of macrophage as well as its inflammatory products (IL-1beta, IL-18, MCP-1alpha, and TNF-alpha) in liver and adipose tissues, which also displayed an obvious inhibition of TLR3/NLRP3 inflammasome molecules. celastrol 27-36 interleukin 1 alpha Mus musculus 116-124 32776627-5 2021 Further studies found that celastrol decreased the infiltration of macrophage as well as its inflammatory products (IL-1beta, IL-18, MCP-1alpha, and TNF-alpha) in liver and adipose tissues, which also displayed an obvious inhibition of TLR3/NLRP3 inflammasome molecules. celastrol 27-36 interleukin 18 Mus musculus 126-131 32776627-5 2021 Further studies found that celastrol decreased the infiltration of macrophage as well as its inflammatory products (IL-1beta, IL-18, MCP-1alpha, and TNF-alpha) in liver and adipose tissues, which also displayed an obvious inhibition of TLR3/NLRP3 inflammasome molecules. celastrol 27-36 tumor necrosis factor Mus musculus 149-158 33130474-0 2021 Celastrol ameliorates Propionibacterium acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 142-147 32776627-5 2021 Further studies found that celastrol decreased the infiltration of macrophage as well as its inflammatory products (IL-1beta, IL-18, MCP-1alpha, and TNF-alpha) in liver and adipose tissues, which also displayed an obvious inhibition of TLR3/NLRP3 inflammasome molecules. celastrol 27-36 toll-like receptor 3 Mus musculus 236-240 32776627-5 2021 Further studies found that celastrol decreased the infiltration of macrophage as well as its inflammatory products (IL-1beta, IL-18, MCP-1alpha, and TNF-alpha) in liver and adipose tissues, which also displayed an obvious inhibition of TLR3/NLRP3 inflammasome molecules. celastrol 27-36 NLR family, pyrin domain containing 3 Mus musculus 241-246 33303989-0 2021 Celastrol induces lipophagy via the LXRalpha/ABCA1 pathway in clear cell renal cell carcinoma. celastrol 0-9 nuclear receptor subfamily 1 group H member 3 Homo sapiens 36-44 33130474-3 2021 PURPOSE: This study aims to investigate whether the inhibition of NLRP3 inflammasome is engaged in the anti-inflammatory activities of celastrol and delineate the underlying mechanism. celastrol 135-144 NLR family pyrin domain containing 3 Homo sapiens 66-71 33130474-4 2021 METHODS: The influence of celastrol on NLRP3 inflammasome activation was firstly studied in lipopolysaccharide (LPS)-primed mouse bone marrow-derived macrophages (BMDMs) and phorbol 12-myristate 13-acetate (PMA)-primed THP-1 cells treated with nigericin. celastrol 26-35 NLR family, pyrin domain containing 3 Mus musculus 39-44 33130474-8 2021 RESULTS: Celastrol significantly suppressed the cleavage of pro-caspase-1 and pro-IL-1beta, while not affecting the protein expressions of NLRP3, ASC, pro-caspase-1 and pro-IL-1beta in THP-1 cells, BMDMs and HEK293T cells. celastrol 9-18 interleukin 1 beta Homo sapiens 78-90 33130474-9 2021 Celastrol suppressed NLRP3 inflammasome activation and alleviated P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 21-26 33130474-10 2021 Mechanism study revealed that celastrol could interdict K63 deubiquitination of NLRP3, which may concern interaction of celastrol and BRCA1/BRCA2-containing complex subunit 3 (BRCC3), and thereby prohibited the formation of NLRP3, ASC and pro-caspase-1 complex to block the generation of mature IL-1beta. celastrol 30-39 NLR family pyrin domain containing 3 Homo sapiens 80-85 33130474-10 2021 Mechanism study revealed that celastrol could interdict K63 deubiquitination of NLRP3, which may concern interaction of celastrol and BRCA1/BRCA2-containing complex subunit 3 (BRCC3), and thereby prohibited the formation of NLRP3, ASC and pro-caspase-1 complex to block the generation of mature IL-1beta. celastrol 30-39 NLR family pyrin domain containing 3 Homo sapiens 224-229 33130474-10 2021 Mechanism study revealed that celastrol could interdict K63 deubiquitination of NLRP3, which may concern interaction of celastrol and BRCA1/BRCA2-containing complex subunit 3 (BRCC3), and thereby prohibited the formation of NLRP3, ASC and pro-caspase-1 complex to block the generation of mature IL-1beta. celastrol 30-39 PYD and CARD domain containing Homo sapiens 231-234 33130474-11 2021 CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases. celastrol 12-21 NLR family pyrin domain containing 3 Homo sapiens 33-38 33130474-11 2021 CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases. celastrol 12-21 NLR family pyrin domain containing 3 Homo sapiens 171-176 33130474-11 2021 CONCLUSION: Celastrol suppresses NLRP3 inflammasome activation in P. acnes/LPS-induced liver damage and MSU-induced gouty arthritis via inhibiting K63 deubiquitination of NLRP3, which presents a novel insight into inhibition of celastrol on NLRP3 inflammasome and provides more evidences for its application in the therapy of inflammation-related diseases. celastrol 12-21 NLR family pyrin domain containing 3 Homo sapiens 171-176 33303989-0 2021 Celastrol induces lipophagy via the LXRalpha/ABCA1 pathway in clear cell renal cell carcinoma. celastrol 0-9 ATP binding cassette subfamily A member 1 Homo sapiens 45-50 33303989-8 2021 Moreover, we revealed that celastrol dramatically activated LXRalpha signaling, and degraded lipid droplets by inducing lipophagy in 786-O cells. celastrol 27-36 nuclear receptor subfamily 1 group H member 3 Homo sapiens 60-68 33303989-9 2021 Finally, celastrol promoted cholesterol efflux from 786-O cells via ABCA1. celastrol 9-18 ATP binding cassette subfamily A member 1 Homo sapiens 68-73 33303989-12 2021 In conclusion, this study reveals that celastrol triggers lipophagy in ccRCC by activating LXRalpha, promotes ABCA1-mediated cholesterol efflux, suppresses EMT progress, and ultimately inhibits cell proliferation, migration, and invasion as well as tumor growth. celastrol 39-48 nuclear receptor subfamily 1 group H member 3 Homo sapiens 91-99 33303989-12 2021 In conclusion, this study reveals that celastrol triggers lipophagy in ccRCC by activating LXRalpha, promotes ABCA1-mediated cholesterol efflux, suppresses EMT progress, and ultimately inhibits cell proliferation, migration, and invasion as well as tumor growth. celastrol 39-48 ATP binding cassette subfamily A member 1 Homo sapiens 110-115 32862144-3 2020 We previously showed that celastrol fitted pharmacophore criteria for activating calcium- and voltage-gated potassium channels of large conductance ("BK") made of subunits cloned from cerebrovascular smooth muscle (SM). celastrol 26-35 synaptotagmin 17 Rattus norvegicus 150-152 33238517-11 2020 Celastrol, a nature extract compound, was demonstrated to effectively inhibit SPC25 expression and reverse CR phenotype. celastrol 0-9 SPC25 component of NDC80 kinetochore complex Homo sapiens 78-83 33238517-12 2020 In conclusion, the development of SPC25 inhibitors, such as the application of celastrol, maybe a novel strategy to sensitize cisplatin for the treatment of refractory HNC. celastrol 79-88 SPC25 component of NDC80 kinetochore complex Homo sapiens 34-39 33250707-8 2020 Both celastrol and indomethacin prevented ketamine-induced enhancement in TNF-alpha and IL-1beta levels, however, they had no effects on increased IL-6 amount resulting from ketamine exposure in postnatal life. celastrol 5-14 tumor necrosis factor Mus musculus 74-83 33250707-8 2020 Both celastrol and indomethacin prevented ketamine-induced enhancement in TNF-alpha and IL-1beta levels, however, they had no effects on increased IL-6 amount resulting from ketamine exposure in postnatal life. celastrol 5-14 interleukin 1 alpha Mus musculus 88-96 32954678-9 2020 Furthermore, celastrol prevented the up-regulation of BMPRII and down-regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. celastrol 13-22 SMAD family member 6 Homo sapiens 84-89 32954678-9 2020 Furthermore, celastrol prevented the up-regulation of BMPRII and down-regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. celastrol 13-22 bone morphogenetic protein 2 Mus musculus 162-166 32954678-10 2020 In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium-induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD. celastrol 60-69 bone morphogenetic protein 2 Homo sapiens 152-156 32954678-10 2020 In conclusion, our data for the first time demonstrate that celastrol attenuates high calcium-induced arterial and valvular calcification by inhibiting BMP2/Smad1/5 signalling, which may provide a novel therapeutic strategy for arterial and valvular calcification in patients with CKD. celastrol 60-69 SMAD family member 1 Homo sapiens 157-164 32781326-1 2020 Palmitic acid-modified bovine serum albumin (PAB) was synthetized and found to own remarkable scavenger receptor-A (SR-A) targeting ability in vitro and in vivo, through which activated macrophages took up PAB nanoparticles (PAB NPs) 9.10 times more than bovine serum albumin nanoparticles (BSA NPs) and PAB NPs could delivery anti-inflammatory drugs celastrol (CLT) to inflamed tissues more effectively than BSA NPs. celastrol 351-360 albumin Rattus norvegicus 30-43 32781326-1 2020 Palmitic acid-modified bovine serum albumin (PAB) was synthetized and found to own remarkable scavenger receptor-A (SR-A) targeting ability in vitro and in vivo, through which activated macrophages took up PAB nanoparticles (PAB NPs) 9.10 times more than bovine serum albumin nanoparticles (BSA NPs) and PAB NPs could delivery anti-inflammatory drugs celastrol (CLT) to inflamed tissues more effectively than BSA NPs. celastrol 362-365 albumin Rattus norvegicus 30-43 32954678-0 2020 Celastrol attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling. celastrol 0-9 bone morphogenetic protein 2 Homo sapiens 72-76 32954678-0 2020 Celastrol attenuates arterial and valvular calcification via inhibiting BMP2/Smad1/5 signalling. celastrol 0-9 SMAD family member 1 Homo sapiens 77-84 32954678-7 2020 At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p-Smad1/5) and non-phosphorylated beta-catenin (n-p-beta-catenin) induced by high-calcium medium both in vitro and in vivo. celastrol 24-33 bone morphogenetic protein 2 Mus musculus 60-64 32954678-7 2020 At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p-Smad1/5) and non-phosphorylated beta-catenin (n-p-beta-catenin) induced by high-calcium medium both in vitro and in vivo. celastrol 24-33 SMAD family member 1 Mus musculus 81-88 32954678-7 2020 At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p-Smad1/5) and non-phosphorylated beta-catenin (n-p-beta-catenin) induced by high-calcium medium both in vitro and in vivo. celastrol 24-33 SMAD family member 1 Mus musculus 92-99 32954678-7 2020 At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p-Smad1/5) and non-phosphorylated beta-catenin (n-p-beta-catenin) induced by high-calcium medium both in vitro and in vivo. celastrol 24-33 catenin beta 1 Homo sapiens 124-136 32954678-7 2020 At the molecular level, celastrol inhibited the increase of BMP2, phosphorylated Smad1/5 (p-Smad1/5) and non-phosphorylated beta-catenin (n-p-beta-catenin) induced by high-calcium medium both in vitro and in vivo. celastrol 24-33 catenin beta 1 Homo sapiens 142-154 32954678-8 2020 Also, BMP2 overexpression reversed the anti-calcification effects of celastrol by recovering the decrease of p-Smad1/5 and n-p-beta-catenin. celastrol 69-78 bone morphogenetic protein 2 Mus musculus 6-10 32954678-8 2020 Also, BMP2 overexpression reversed the anti-calcification effects of celastrol by recovering the decrease of p-Smad1/5 and n-p-beta-catenin. celastrol 69-78 SMAD family member 1 Mus musculus 111-118 32954678-8 2020 Also, BMP2 overexpression reversed the anti-calcification effects of celastrol by recovering the decrease of p-Smad1/5 and n-p-beta-catenin. celastrol 69-78 catenin beta 1 Homo sapiens 127-139 32954678-9 2020 Furthermore, celastrol prevented the up-regulation of BMPRII and down-regulation of Smad6 induced by high calcium, and this protectory effect can be abolished by BMP2 overexpression. celastrol 13-22 bone morphogenetic protein receptor type 2 Homo sapiens 54-60 32862144-8 2020 Selective BK block with 1 microM paxilline blunts celastrol vasodilation. celastrol 50-59 synaptotagmin 17 Rattus norvegicus 10-12 32862144-11 2020 MCA constriction by ethanol concentrations reached in blood during moderate-heavy alcohol drinking (50 mM), which involves SM BK inhibition, is both prevented and reverted by celastrol. celastrol 175-184 synaptotagmin 17 Rattus norvegicus 126-128 32862144-12 2020 We conclude that celastrol could be an effective cerebrovascular dilator and antagonist of alcohol-induced cerebrovascular constriction, its efficacy being uncompromised by conditions that disrupt endothelial and/or BK function. celastrol 17-26 synaptotagmin 17 Rattus norvegicus 216-218 32862144-14 2020 Celastrol actions are endothelium-independent but mediated through voltage-gated potassium and calcium/voltage-gated, big-conductance (BK) potassium channels. celastrol 0-9 synaptotagmin 17 Rattus norvegicus 135-137 33097050-0 2020 Celastrol slows the progression of early diabetic nephropathy in rats via the PI3K/AKT pathway. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 83-86 33097050-5 2020 RESULTS: High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-kappaB and mTOR. celastrol 22-31 microtubule-associated protein 1 light chain 3 alpha Rattus norvegicus 214-219 33097050-5 2020 RESULTS: High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-kappaB and mTOR. celastrol 22-31 NPHS1 adhesion molecule, nephrin Rattus norvegicus 224-231 33097050-5 2020 RESULTS: High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-kappaB and mTOR. celastrol 22-31 AKT serine/threonine kinase 1 Rattus norvegicus 277-280 33097050-5 2020 RESULTS: High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-kappaB and mTOR. celastrol 22-31 mechanistic target of rapamycin kinase Rattus norvegicus 318-322 33097050-6 2020 CONCLUSION: Celastrol functions as a potential therapeutic substance, acting via the PI3K/AKT pathway to attenuate renal injury, inhibit glomerular basement membrane thickening, and achieve podocyte homeostasis in diabetic nephropathy. celastrol 12-21 AKT serine/threonine kinase 1 Rattus norvegicus 90-93 32920591-0 2020 Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-kappaB (NF-kappaB). celastrol 0-9 interleukin 6 Homo sapiens 96-109 32965124-0 2020 Inflammation-targeted celastrol nanodrug attenuates collagen-induced arthritis through NF-kappaB and Notch1 pathways. celastrol 22-31 nuclear factor kappa B subunit 1 Homo sapiens 87-96 32965124-0 2020 Inflammation-targeted celastrol nanodrug attenuates collagen-induced arthritis through NF-kappaB and Notch1 pathways. celastrol 22-31 notch receptor 1 Homo sapiens 101-107 32431112-5 2020 We then treated leptin knockout rats with celastrol and explored the changes in energy metabolism. celastrol 42-51 leptin Rattus norvegicus 16-22 32431112-9 2020 Hypothalamic transcriptome analysis showed a significant enrichment of the leptin signaling pathway, and we found that celastrol significantly enhanced energy expenditure, which was mediated by the leptin signaling pathway. celastrol 119-128 leptin Mus musculus 198-204 32431112-11 2020 CONCLUSION: Our study revealed that celastrol decreased the BW of obese rats by enhancing energy expenditure but not by suppressing food intake and that this effect was mediated by the improvement of the gut microbiota and the activation of the hypothalamic leptin signaling pathway. celastrol 36-45 leptin Rattus norvegicus 258-264 32818610-3 2020 Therefore, we aimed in this study is to combine the merits of NF-kappaB inhibiting potential of celastrol (CST) with glutathione inhibitory effect of sulfasalazine (SFZ) which prevents CST inactivation and thus enhances its anti-tumor activity. celastrol 96-105 nuclear factor kappa B subunit 1 Homo sapiens 62-71 32712089-0 2020 Celastrol attenuates inflammatory responses in adipose tissues and improves skeletal muscle mitochondrial functions in high fat diet-induced obese rats via upregulation of AMPK/SIRT1 signaling pathways. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 172-176 32712089-0 2020 Celastrol attenuates inflammatory responses in adipose tissues and improves skeletal muscle mitochondrial functions in high fat diet-induced obese rats via upregulation of AMPK/SIRT1 signaling pathways. celastrol 0-9 sirtuin 1 Rattus norvegicus 177-182 32712089-6 2020 Celastrol noticeably improved insulin-stimulated glucose uptake activity and increased expression of plasma membrane GLUT4 protein in skeletal muscle. celastrol 0-9 solute carrier family 2 member 4 Rattus norvegicus 117-122 32712089-9 2020 Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. celastrol 17-26 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 97-145 32712089-9 2020 Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. celastrol 17-26 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 147-151 32712089-9 2020 Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. celastrol 17-26 sirtuin 1 Rattus norvegicus 157-166 32712089-9 2020 Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. celastrol 17-26 sirtuin 1 Rattus norvegicus 168-173 33096778-7 2020 Consequently, we identified amphotericin B and celastrol as new non-substrate-based XT-I protein inhibitors. celastrol 47-56 xylosyltransferase 1 Homo sapiens 84-88 33282271-7 2020 Celastrol had effects to depress TG, TC, LDL-C, GPT, GOT, and MDA concentration and increase HDL-C and SOD concentration (p < .05, respectively) with dose-dependent. celastrol 0-9 glutamic pyruvic transaminase, soluble Mus musculus 48-51 33282271-10 2020 Celastrol can inhibit the oxidative stress reaction and liver cell apoptosis via regulation Nrf2/HO-1 pathway in T2DM mice with NAFLD. celastrol 0-9 nuclear factor, erythroid derived 2, like 2 Mus musculus 92-96 33282271-10 2020 Celastrol can inhibit the oxidative stress reaction and liver cell apoptosis via regulation Nrf2/HO-1 pathway in T2DM mice with NAFLD. celastrol 0-9 heme oxygenase 1 Mus musculus 97-101 32920591-0 2020 Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-kappaB (NF-kappaB). celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 129-150 32920591-0 2020 Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-kappaB (NF-kappaB). celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 152-161 32920591-5 2020 The expression of interleukin-6 (IL-6) was measured after transfection of short-hairpin RNA against IL-6 or celastrol treatment via quantitative real-time polymerase chain reaction, Western blot, or enzyme-linked immunosorbent analysis (ELISA). celastrol 108-117 interleukin 6 Homo sapiens 18-31 32920591-5 2020 The expression of interleukin-6 (IL-6) was measured after transfection of short-hairpin RNA against IL-6 or celastrol treatment via quantitative real-time polymerase chain reaction, Western blot, or enzyme-linked immunosorbent analysis (ELISA). celastrol 108-117 interleukin 6 Homo sapiens 33-37 32920591-7 2020 The interaction between celastrol and NF-kappaB-mediated IL-6 was investigated by luciferase reporter assay. celastrol 24-33 nuclear factor kappa B subunit 1 Homo sapiens 38-47 32920591-7 2020 The interaction between celastrol and NF-kappaB-mediated IL-6 was investigated by luciferase reporter assay. celastrol 24-33 interleukin 6 Homo sapiens 57-61 32920591-10 2020 Moreover, treatment with celastrol decreased IL-6 expression at mRNA and protein levels. celastrol 25-34 interleukin 6 Homo sapiens 45-49 32920591-11 2020 IL-6 overexpression mitigated celastrol-mediated suppression of cell migration and invasion. celastrol 30-39 interleukin 6 Homo sapiens 0-4 32920591-12 2020 Additionally, celastrol blocked the NF-kappaB pathway to inhibit IL-6 levels. celastrol 14-23 nuclear factor kappa B subunit 1 Homo sapiens 36-45 32920591-12 2020 Additionally, celastrol blocked the NF-kappaB pathway to inhibit IL-6 levels. celastrol 14-23 interleukin 6 Homo sapiens 65-69 32920591-13 2020 CONCLUSIONS Celastrol repressed migration and invasion through decreasing IL-6 levels by inactivation of NF-kappaB signaling in triple-negative breast cancer cells, providing a novel basis for use of celastrol in treating triple-negative breast cancer. celastrol 12-21 interleukin 6 Homo sapiens 74-78 32920591-13 2020 CONCLUSIONS Celastrol repressed migration and invasion through decreasing IL-6 levels by inactivation of NF-kappaB signaling in triple-negative breast cancer cells, providing a novel basis for use of celastrol in treating triple-negative breast cancer. celastrol 12-21 nuclear factor kappa B subunit 1 Homo sapiens 105-114 32920591-13 2020 CONCLUSIONS Celastrol repressed migration and invasion through decreasing IL-6 levels by inactivation of NF-kappaB signaling in triple-negative breast cancer cells, providing a novel basis for use of celastrol in treating triple-negative breast cancer. celastrol 200-209 interleukin 6 Homo sapiens 74-78 32920591-13 2020 CONCLUSIONS Celastrol repressed migration and invasion through decreasing IL-6 levels by inactivation of NF-kappaB signaling in triple-negative breast cancer cells, providing a novel basis for use of celastrol in treating triple-negative breast cancer. celastrol 200-209 nuclear factor kappa B subunit 1 Homo sapiens 105-114 32307774-0 2020 Celastrol mitigates high glucose-induced inflammation and apoptosis in rat H9c2 cardiomyocytes via miR-345-5p/growth arrest-specific 6. celastrol 0-9 growth arrest specific 6 Rattus norvegicus 99-134 32524263-3 2020 After treatment with poly(I:C)-LMW, poly (I:C)-LMW/LyoVec, and Imiquimod, the replication of IBV was significantly suppressed after 24 h. However, treatment with TLR3 pathway inhibitors such as Pepinh-TRIF, celastrol, chloroquine, and BX795 resulted in increased replication of IBV after 36 h. These results also showed that chloroquine and celastrol were most effective inhibitors of the antiviral response at 48 hpi. celastrol 207-216 toll like receptor 3 Homo sapiens 162-166 32524263-3 2020 After treatment with poly(I:C)-LMW, poly (I:C)-LMW/LyoVec, and Imiquimod, the replication of IBV was significantly suppressed after 24 h. However, treatment with TLR3 pathway inhibitors such as Pepinh-TRIF, celastrol, chloroquine, and BX795 resulted in increased replication of IBV after 36 h. These results also showed that chloroquine and celastrol were most effective inhibitors of the antiviral response at 48 hpi. celastrol 341-350 toll like receptor 3 Homo sapiens 162-166 33015082-8 2020 Results: Doses higher than 2.5 mug/g/day of celastrol reduced the inflammatory score and ankle swelling, preserved joint structure, halted bone destruction, and diminished the number of synovial CD68+ macrophages. celastrol 44-53 Cd68 molecule Rattus norvegicus 195-199 32649040-8 2020 Importantly, the addition of resveratrol upregulated the proliferation of HPLF cells, while osteoclastogenesis of BMM cells treated with mCSF-RANKL was significantly downregulated by celastrol. celastrol 183-192 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 137-141 32649040-8 2020 Importantly, the addition of resveratrol upregulated the proliferation of HPLF cells, while osteoclastogenesis of BMM cells treated with mCSF-RANKL was significantly downregulated by celastrol. celastrol 183-192 TNF superfamily member 11 Homo sapiens 142-147 32307774-9 2020 Moreover, Cel exhibited the ability to antagonize HG-induced cardiomyocyte apoptosis and suppress the elevated Bax/Bcl-2 ratio elicited by HG stimulation. celastrol 10-13 BCL2 associated X, apoptosis regulator Rattus norvegicus 111-114 32307774-9 2020 Moreover, Cel exhibited the ability to antagonize HG-induced cardiomyocyte apoptosis and suppress the elevated Bax/Bcl-2 ratio elicited by HG stimulation. celastrol 10-13 BCL2, apoptosis regulator Rattus norvegicus 115-120 32307774-10 2020 Intriguingly, Cel treatment revoked the HG-triggered repression of Gas6 protein expression, and Gas6 loss-of-function accelerated HG-induced cardiomyocyte apoptosis. celastrol 14-17 growth arrest specific 6 Rattus norvegicus 67-71 32307774-14 2020 CONCLUSIONS: Our findings have demonstrated that Cel administration antagonized HG-induced cardiomyocyte apoptosis and inflammation through upregulating Gas6 expression by restraining miR-345-5p. celastrol 49-52 growth arrest specific 6 Rattus norvegicus 153-157 32848589-0 2020 Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-kappaB Signaling Pathway. celastrol 27-36 high mobility group box 1 Rattus norvegicus 95-100 32815304-6 2020 Through suppressing the phosphorylation of upstream EGFR and downstream Akt in the EGFR pathway by gefitinib and celastrol, respectively, the nanodrug exhibits high inhibition efficacy against orthotopic NSCLC in mouse models. celastrol 113-122 epidermal growth factor receptor Mus musculus 52-56 32815304-6 2020 Through suppressing the phosphorylation of upstream EGFR and downstream Akt in the EGFR pathway by gefitinib and celastrol, respectively, the nanodrug exhibits high inhibition efficacy against orthotopic NSCLC in mouse models. celastrol 113-122 thymoma viral proto-oncogene 1 Mus musculus 72-75 32815304-6 2020 Through suppressing the phosphorylation of upstream EGFR and downstream Akt in the EGFR pathway by gefitinib and celastrol, respectively, the nanodrug exhibits high inhibition efficacy against orthotopic NSCLC in mouse models. celastrol 113-122 epidermal growth factor receptor Mus musculus 83-87 32929349-0 2020 Celastrol induces ROS-mediated apoptosis via directly targeting peroxiredoxin-2 in gastric cancer cells. celastrol 0-9 peroxiredoxin 2 Homo sapiens 64-79 32929349-8 2020 Results: Our data show that Celastrol directly binds to an antioxidant enzyme, peroxiredoxin-2 (Prdx2), which then inhibits its enzyme activity at both molecular and cellular level. celastrol 28-37 peroxiredoxin 2 Homo sapiens 79-94 32929349-8 2020 Results: Our data show that Celastrol directly binds to an antioxidant enzyme, peroxiredoxin-2 (Prdx2), which then inhibits its enzyme activity at both molecular and cellular level. celastrol 28-37 peroxiredoxin 2 Mus musculus 96-101 32929349-9 2020 Inhibition of Prdx2 by Celastrol increased cellular ROS levels and led to ROS-dependent endoplasmic reticulum stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells. celastrol 23-32 peroxiredoxin 2 Mus musculus 14-19 32929349-10 2020 Functional tests demonstrated that Celastrol limits gastric cancer cells, at least in part, through targeting Prdx2. celastrol 35-44 peroxiredoxin 2 Mus musculus 110-115 32929349-11 2020 Celastrol treatment of mice implanted with gastric cancer cells also inhibited tumor growth, associated with Prdx2 inhibition and increased ROS. celastrol 0-9 peroxiredoxin 2 Mus musculus 109-114 32929349-13 2020 Conclusion: Our studies have uncovered a potential Celastrol-interacting protein Prdx2 and a ROS-dependent mechanism of its action. celastrol 51-60 peroxiredoxin 2 Homo sapiens 81-86 32848589-6 2020 Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-alpha, IL-1beta, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. celastrol 27-36 tumor necrosis factor Rattus norvegicus 127-136 32848589-6 2020 Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-alpha, IL-1beta, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. celastrol 27-36 interleukin 1 alpha Rattus norvegicus 138-146 32848589-6 2020 Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-alpha, IL-1beta, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. celastrol 27-36 interleukin 6 Rattus norvegicus 152-156 32848589-6 2020 Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-alpha, IL-1beta, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. celastrol 27-36 interleukin 10 Rattus norvegicus 230-235 32848589-6 2020 Our results indicated that celastrol dose-dependently reduced hippocampal and serum concentration of pro-inflammatory markers (TNF-alpha, IL-1beta, and IL-6) and oxidative stress marker (MDA), whereas the anti-inflammatory marker IL-10 and antioxidant markers (GSH, SOD, and CAT) were increased significantly in celastrol treated tGCI/R rats. celastrol 27-36 catalase Rattus norvegicus 275-278 32848589-8 2020 Simultaneously, we found that mechanisms responsible for the neuroprotective effect of celastrol could be attributed to its anti-inflammatory and antioxidant actions via inhibiting HMGB1/NF-kappaB signaling pathway. celastrol 87-96 high mobility group box 1 Rattus norvegicus 181-186 32953791-10 2020 After the addition of celastrol, MCL treatment significantly reduced the levels of p-p65, NLRP3, caspase-1, and ASC. celastrol 22-31 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 85-88 32953791-10 2020 After the addition of celastrol, MCL treatment significantly reduced the levels of p-p65, NLRP3, caspase-1, and ASC. celastrol 22-31 NLR family, pyrin domain containing 3 Mus musculus 90-95 32953791-10 2020 After the addition of celastrol, MCL treatment significantly reduced the levels of p-p65, NLRP3, caspase-1, and ASC. celastrol 22-31 caspase 1 Mus musculus 97-106 32953791-10 2020 After the addition of celastrol, MCL treatment significantly reduced the levels of p-p65, NLRP3, caspase-1, and ASC. celastrol 22-31 PYD and CARD domain containing Mus musculus 112-115 32565148-0 2020 Celastrol ameliorates autoimmune disorders in Trex1-deficient mice. celastrol 0-9 three prime repair exonuclease 1 Mus musculus 46-51 32470546-0 2020 Celastrol ameliorates acute liver injury through modulation of PPARalpha. celastrol 0-9 peroxisome proliferator activated receptor alpha Mus musculus 63-72 32470546-2 2020 In the present study, the protective effect of celastrol on carbon tetrachloride (CCl4)-induced acute liver injury was investigated. celastrol 47-56 chemokine (C-C motif) ligand 4 Mus musculus 82-86 32470546-3 2020 Celastrol improved the increased transaminase activity, inflammation, and oxidative stress induced by CCl4, resulting in improved metabolic disorders found in mice with liver injury. celastrol 0-9 chemokine (C-C motif) ligand 4 Mus musculus 102-106 32470546-4 2020 Dual-luciferase reporter assays and primary hepatocyte studies demonstrated that the peroxisome proliferator-activated receptor alpha (PPARalpha) signaling mediated the protective effect of celastrol, which was not observed in Ppara-null mice, and co-treatment of wild-type mice with the PPARalpha antagonist GW6471. celastrol 190-199 peroxisome proliferator activated receptor alpha Mus musculus 85-133 32470546-4 2020 Dual-luciferase reporter assays and primary hepatocyte studies demonstrated that the peroxisome proliferator-activated receptor alpha (PPARalpha) signaling mediated the protective effect of celastrol, which was not observed in Ppara-null mice, and co-treatment of wild-type mice with the PPARalpha antagonist GW6471. celastrol 190-199 peroxisome proliferator activated receptor alpha Mus musculus 135-144 32470546-4 2020 Dual-luciferase reporter assays and primary hepatocyte studies demonstrated that the peroxisome proliferator-activated receptor alpha (PPARalpha) signaling mediated the protective effect of celastrol, which was not observed in Ppara-null mice, and co-treatment of wild-type mice with the PPARalpha antagonist GW6471. celastrol 190-199 peroxisome proliferator activated receptor alpha Mus musculus 288-297 32470546-6 2020 These data demonstrate a novel role for celastrol in protection against acute liver injury through modulating PPARalpha signaling. celastrol 40-49 peroxisome proliferator activated receptor alpha Mus musculus 110-119 32565148-3 2020 Here we showed that celastrol caused inhibition of interferon regulatory factor 3 (IRF3) activation leading to the down-regulation of the interferon response triggered by cytosolic nucleic acids in vitro and in vivo. celastrol 20-29 interferon regulatory factor 3 Mus musculus 51-81 32565148-3 2020 Here we showed that celastrol caused inhibition of interferon regulatory factor 3 (IRF3) activation leading to the down-regulation of the interferon response triggered by cytosolic nucleic acids in vitro and in vivo. celastrol 20-29 interferon regulatory factor 3 Mus musculus 83-87 32565148-4 2020 Moreover, celastrol treatment markedly ameliorates the autoimmune phenotypes including myocarditis, aberrant interferon response and autoantibody production, as well as the excessive T-cell activation in Trex1-/- autoimmune disease mouse model. celastrol 10-19 three prime repair exonuclease 1 Mus musculus 204-209 32565148-5 2020 Collectively, our results indicate that celastrol inhibits interferon response by targeting IRF3 activation and may be used as an effective treatment for interferon response-dependent autoimmune diseases. celastrol 40-49 interferon regulatory factor 3 Mus musculus 92-96 32470352-0 2020 Celastrol augments sensitivity of NLRP3 to CP-456773 by modulating HSP-90 and inducing autophagy in dextran sodium sulphate-induced colitis in rats. celastrol 0-9 NLR family, pyrin domain containing 3 Rattus norvegicus 34-39 31065693-10 2020 In an in vivo iKspCre-Pkd1lox,lox mouse model for PKD, celastrol inhibited the growth of renal cysts and maintained kidney function. celastrol 55-64 lysyl oxidase Mus musculus 26-29 32470352-0 2020 Celastrol augments sensitivity of NLRP3 to CP-456773 by modulating HSP-90 and inducing autophagy in dextran sodium sulphate-induced colitis in rats. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 67-73 32201950-0 2020 Celastrol ameliorates endoplasmic stress-mediated apoptosis of osteoarthritis via regulating ATF-6/CHOP signalling pathway. celastrol 0-9 activating transcription factor 6 Rattus norvegicus 93-98 32723973-4 2020 Mechanistically, Celastrol was able to control the differentiation of BM-MSCs by stimulating PGC-1alpha signaling. celastrol 17-26 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 93-103 32647287-10 2020 Our findings suggest that targeting ROCK2-ezrin signaling is a potential therapeutic niche for celastrol-based intervention of cancer progression in hepatocellular carcinoma. celastrol 95-104 ezrin Homo sapiens 42-47 32222543-6 2020 Celastrol treatment led to a significant increase in mutant PMM2 protein concentration and activity, while MG132 had a small effect on protein concentration only. celastrol 0-9 phosphomannomutase 2 Homo sapiens 60-64 32902404-9 2020 Tripterine administration induced the growth inhibition of NIH/3T3 cells indicated by a trend toward the decreased expression of matrix metallopeptidase (MMPs), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). celastrol 0-10 vascular endothelial growth factor A Mus musculus 161-195 32902404-9 2020 Tripterine administration induced the growth inhibition of NIH/3T3 cells indicated by a trend toward the decreased expression of matrix metallopeptidase (MMPs), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). celastrol 0-10 vascular endothelial growth factor A Mus musculus 197-201 32902404-9 2020 Tripterine administration induced the growth inhibition of NIH/3T3 cells indicated by a trend toward the decreased expression of matrix metallopeptidase (MMPs), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). celastrol 0-10 fibroblast growth factor 2 Mus musculus 207-237 32902404-9 2020 Tripterine administration induced the growth inhibition of NIH/3T3 cells indicated by a trend toward the decreased expression of matrix metallopeptidase (MMPs), vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). celastrol 0-10 fibroblast growth factor 2 Mus musculus 239-243 32902404-13 2020 Tripterine exhibited an anti-scarring bioactivity in NIH/3T3 cells by inhibiting ANRIL, and this process was accompanied by the blockade of nuclear factor-kappa B (NF-kappaB) and beta-catenin cascades. celastrol 0-10 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 140-162 32902404-13 2020 Tripterine exhibited an anti-scarring bioactivity in NIH/3T3 cells by inhibiting ANRIL, and this process was accompanied by the blockade of nuclear factor-kappa B (NF-kappaB) and beta-catenin cascades. celastrol 0-10 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 164-173 32902404-13 2020 Tripterine exhibited an anti-scarring bioactivity in NIH/3T3 cells by inhibiting ANRIL, and this process was accompanied by the blockade of nuclear factor-kappa B (NF-kappaB) and beta-catenin cascades. celastrol 0-10 catenin (cadherin associated protein), beta 1 Mus musculus 179-191 32723973-6 2020 Together, these results recommended that Celastrol could regulate BM-MSCs fate and bone-fat balance in OP and skeletal aging by stimulating PGC-1alpha, which might act as a possible therapeutic target for OP and for the prevention of skeletal aging. celastrol 41-50 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 140-150 32647287-0 2020 Celastrol inhibits ezrin-mediated migration of hepatocellular carcinoma cells. celastrol 0-9 ezrin Homo sapiens 19-24 32647287-5 2020 Here we show that ROCK2 is a novel target of celastrol and inhibition of ROCK2 suppresses elicited ezrin activation and liver cancer cell migration. celastrol 45-54 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 18-23 32647287-5 2020 Here we show that ROCK2 is a novel target of celastrol and inhibition of ROCK2 suppresses elicited ezrin activation and liver cancer cell migration. celastrol 45-54 ezrin Homo sapiens 99-104 32647287-7 2020 The molecular target of celastrol was identified as ROCK2 using celastrol affinity pull-down assay. celastrol 24-33 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 52-57 32647287-7 2020 The molecular target of celastrol was identified as ROCK2 using celastrol affinity pull-down assay. celastrol 64-73 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 52-57 32647287-8 2020 Our molecular docking analyses indicated celastrol binds to the active site of ROCK2 kinase. celastrol 41-50 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 79-84 32647287-9 2020 Mechanistically, celastrol inhibits the ROCK2-mediated phosphorylation of ezrin at Thr567 which harnesses liver cancer cell migration. celastrol 17-26 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 40-45 32647287-9 2020 Mechanistically, celastrol inhibits the ROCK2-mediated phosphorylation of ezrin at Thr567 which harnesses liver cancer cell migration. celastrol 17-26 ezrin Homo sapiens 74-79 32647287-10 2020 Our findings suggest that targeting ROCK2-ezrin signaling is a potential therapeutic niche for celastrol-based intervention of cancer progression in hepatocellular carcinoma. celastrol 95-104 Rho associated coiled-coil containing protein kinase 2 Homo sapiens 36-41 32222543-7 2020 The increase in enzymatic activity with celastrol correlated with an increase in the transcriptional and proteome levels of the heat shock proteins Hsp90 and Hsp70. celastrol 40-49 heat shock protein 90 alpha family class A member 1 Homo sapiens 148-153 32222543-7 2020 The increase in enzymatic activity with celastrol correlated with an increase in the transcriptional and proteome levels of the heat shock proteins Hsp90 and Hsp70. celastrol 40-49 heat shock protein family A (Hsp70) member 4 Homo sapiens 158-163 32222543-8 2020 The use of specific Hsp70 or Hsp90 inhibitors showed the positive effect of celastrol on PMM2 stability and activity to occur through Hsp90-driven modulation of the proteostasis network. celastrol 76-85 heat shock protein family A (Hsp70) member 4 Homo sapiens 20-25 32222543-8 2020 The use of specific Hsp70 or Hsp90 inhibitors showed the positive effect of celastrol on PMM2 stability and activity to occur through Hsp90-driven modulation of the proteostasis network. celastrol 76-85 heat shock protein 90 alpha family class A member 1 Homo sapiens 29-34 32222543-8 2020 The use of specific Hsp70 or Hsp90 inhibitors showed the positive effect of celastrol on PMM2 stability and activity to occur through Hsp90-driven modulation of the proteostasis network. celastrol 76-85 phosphomannomutase 2 Homo sapiens 89-93 32222543-8 2020 The use of specific Hsp70 or Hsp90 inhibitors showed the positive effect of celastrol on PMM2 stability and activity to occur through Hsp90-driven modulation of the proteostasis network. celastrol 76-85 heat shock protein 90 alpha family class A member 1 Homo sapiens 134-139 32222543-9 2020 The synergistic effect of celastrol and a previously described pharmacological chaperone was also examined, and a mutation-dependent synergistic effect on PMM2 activity was noted. celastrol 26-35 phosphomannomutase 2 Homo sapiens 155-159 32402948-7 2020 The increased levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and interferon (IFN)-gamma, were abolished by celastrol treatment. celastrol 167-176 tumor necrosis factor Rattus norvegicus 56-89 32402948-7 2020 The increased levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and interferon (IFN)-gamma, were abolished by celastrol treatment. celastrol 167-176 interleukin 1 alpha Rattus norvegicus 91-113 32402948-7 2020 The increased levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and interferon (IFN)-gamma, were abolished by celastrol treatment. celastrol 167-176 interleukin 6 Rattus norvegicus 115-119 32402948-7 2020 The increased levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and interferon (IFN)-gamma, were abolished by celastrol treatment. celastrol 167-176 interferon gamma Rattus norvegicus 125-147 32402948-9 2020 Nox4 overexpression reversed the attenuating effects of celastrol on paw swelling and arthritis scores in CIA rats. celastrol 56-65 NADPH oxidase 4 Rattus norvegicus 0-4 32402948-10 2020 The celastrol-induced improvement in spleen and thymus indexes in CIA rats was inhibited by Nox4 overexpression. celastrol 4-13 NADPH oxidase 4 Rattus norvegicus 92-96 32402948-11 2020 Nox4 overexpression reversed the abolishing effects of celastrol on the increases of TNF-alpha, IL-1beta, IL-6, and IFN-gamma levels in the serum of CIA rats. celastrol 55-64 NADPH oxidase 4 Rattus norvegicus 0-4 32402948-11 2020 Nox4 overexpression reversed the abolishing effects of celastrol on the increases of TNF-alpha, IL-1beta, IL-6, and IFN-gamma levels in the serum of CIA rats. celastrol 55-64 tumor necrosis factor Rattus norvegicus 85-94 32402948-11 2020 Nox4 overexpression reversed the abolishing effects of celastrol on the increases of TNF-alpha, IL-1beta, IL-6, and IFN-gamma levels in the serum of CIA rats. celastrol 55-64 interleukin 1 alpha Rattus norvegicus 96-104 32402948-11 2020 Nox4 overexpression reversed the abolishing effects of celastrol on the increases of TNF-alpha, IL-1beta, IL-6, and IFN-gamma levels in the serum of CIA rats. celastrol 55-64 interleukin 6 Rattus norvegicus 106-110 32402948-11 2020 Nox4 overexpression reversed the abolishing effects of celastrol on the increases of TNF-alpha, IL-1beta, IL-6, and IFN-gamma levels in the serum of CIA rats. celastrol 55-64 interferon gamma Rattus norvegicus 116-125 32201950-0 2020 Celastrol ameliorates endoplasmic stress-mediated apoptosis of osteoarthritis via regulating ATF-6/CHOP signalling pathway. celastrol 0-9 DNA-damage inducible transcript 3 Rattus norvegicus 99-103 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 caspase 3 Rattus norvegicus 60-69 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 caspase 6 Rattus norvegicus 71-80 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 caspase 9 Rattus norvegicus 85-94 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 growth differentiation factor 10 Rattus norvegicus 106-109 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 activating transcription factor 6 Rattus norvegicus 111-115 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 DNA-damage inducible transcript 3 Rattus norvegicus 117-121 32201950-9 2020 Celastrol reduced enzyme activity and protein expression of caspase-3, caspase-6 and caspase-9, decreased Bip, Atf6, Chop and Xbp-1 expression both at protein and mRNA levels. celastrol 0-9 X-box binding protein 1 Rattus norvegicus 126-131 32277035-8 2020 NRF2 is a celastrol target expressed in the habenula (HB), known to play a critical role in the pathophysiology of depression. celastrol 10-19 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4 32237164-5 2020 Herein, we present a microfluidic 3D co-flow device to generate human serum albumin/celastrol nanoparticles by co-flowing an aqueous protein solution with celastrol in ethanol. celastrol 84-93 albumin Homo sapiens 70-83 32237164-5 2020 Herein, we present a microfluidic 3D co-flow device to generate human serum albumin/celastrol nanoparticles by co-flowing an aqueous protein solution with celastrol in ethanol. celastrol 155-164 albumin Homo sapiens 70-83 32098592-0 2020 Celastrol Attenuates Angiotensin II-Induced Cardiac Remodeling by Targeting STAT3. celastrol 0-9 angiotensinogen Rattus norvegicus 21-35 32098592-0 2020 Celastrol Attenuates Angiotensin II-Induced Cardiac Remodeling by Targeting STAT3. celastrol 0-9 signal transducer and activator of transcription 3 Rattus norvegicus 76-81 32098592-3 2020 Objective: We have examined the potential effect of Celastrol, a bioactive compound derived from the Celastraceae family, on Ang II-induced cardiac dysfunction. celastrol 52-61 angiotensinogen Rattus norvegicus 125-131 32098592-4 2020 Methods and Results: In rat primary cardiomyocytes and H9C2 cells, Celastrol attenuates Ang II-induced cellular hypertrophy and fibrotic responses. celastrol 67-76 angiotensinogen Rattus norvegicus 88-94 31931051-0 2020 Targeted delivery of celastrol to renal interstitial myofibroblasts using fibronectin-binding liposomes attenuates renal fibrosis and reduces systemic toxicity. celastrol 21-30 fibronectin 1 Mus musculus 74-85 32098592-6 2020 Our data showed that Celastrol directly binds to and inhibits signal transducer and activator of transcription-3 (STAT3) phosphorylation and nuclear translocation. celastrol 21-30 signal transducer and activator of transcription 3 Rattus norvegicus 62-112 32098592-6 2020 Our data showed that Celastrol directly binds to and inhibits signal transducer and activator of transcription-3 (STAT3) phosphorylation and nuclear translocation. celastrol 21-30 signal transducer and activator of transcription 3 Rattus norvegicus 114-119 32098592-7 2020 Functional tests demonstrated that the protection of Celastrol is afforded through targeting STAT3. celastrol 53-62 signal transducer and activator of transcription 3 Rattus norvegicus 93-98 32098592-8 2020 Overexpression of STAT3 dampens the effect of Celastrol by partially rescuing STAT3 activity. celastrol 46-55 signal transducer and activator of transcription 3 Rattus norvegicus 18-23 32098592-8 2020 Overexpression of STAT3 dampens the effect of Celastrol by partially rescuing STAT3 activity. celastrol 46-55 signal transducer and activator of transcription 3 Rattus norvegicus 78-83 32098592-9 2020 Finally, we investigated the in vivo effect of Celastrol treatment in mice challenged with Ang II and in the Transverse aortic constriction (TAC) model. celastrol 47-56 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 91-97 32098592-10 2020 We show that Celastrol administration protected heart function in Ang II- and TAC-challenged mice by inhibiting cardiac fibrosis and hypertrophy. celastrol 13-22 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 66-72 32098592-11 2020 Conclusions: Our studies show that Celastrol inhibits Ang II-induced cardiac dysfunction by inhibiting STAT3 activity. celastrol 35-44 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 54-60 32098592-11 2020 Conclusions: Our studies show that Celastrol inhibits Ang II-induced cardiac dysfunction by inhibiting STAT3 activity. celastrol 35-44 signal transducer and activator of transcription 3 Rattus norvegicus 103-108 31904241-0 2020 Celastrol-loaded galactosylated liposomes effectively inhibit AKT/c-Met-triggered rapid hepatocarcinogenesis in mice. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 62-65 32308429-0 2020 Tripterine Restrains the Aggressiveness of Hepatocellular Carcinoma Cell via Regulating miRNA-532-5p/CXCL2 Axis. celastrol 0-10 C-X-C motif chemokine ligand 2 Homo sapiens 101-106 32308429-10 2020 Under tripterine treatment, the level of miR-532-5p was strikingly raised, and overexpression of miR-532-5p reduced cell viability and metastatic-related traits. celastrol 6-16 microRNA 532 Homo sapiens 41-48 32308429-12 2020 Rescue experiments indicated that overexpression of CXCL2 restored the migration and invasive capacity of HCC cells inhibited by miR-532-5p or tripterine treatment. celastrol 143-153 C-X-C motif chemokine ligand 2 Homo sapiens 52-57 32308429-14 2020 The expression of CXCL2 was distinctly decreased and miR-532-5p level was increased by tripterine in vivo. celastrol 87-97 C-X-C motif chemokine ligand 2 Homo sapiens 18-23 32308429-15 2020 Conclusion: In conclusion, tripterine inhibits the growth, migration ability and invasiveness of HCC cells through intervening miR-532-5p/CXCL2. celastrol 27-37 microRNA 532 Homo sapiens 127-134 32308429-15 2020 Conclusion: In conclusion, tripterine inhibits the growth, migration ability and invasiveness of HCC cells through intervening miR-532-5p/CXCL2. celastrol 27-37 C-X-C motif chemokine ligand 2 Homo sapiens 138-143 32112120-8 2020 RESULTS: We found celastrol ameliorated IL-1beta-induced chondrocyte apoptosis and increased the expression of LC3-II and Beclin-1. celastrol 18-27 interleukin 1 alpha Rattus norvegicus 40-48 32112120-8 2020 RESULTS: We found celastrol ameliorated IL-1beta-induced chondrocyte apoptosis and increased the expression of LC3-II and Beclin-1. celastrol 18-27 beclin 1 Rattus norvegicus 122-130 32112120-10 2020 Moreover, celastrol decreased the IL-1beta-stimulated phosphorylation degree of IkappaBalpha and P65. celastrol 10-19 interleukin 1 alpha Rattus norvegicus 34-42 32112120-10 2020 Moreover, celastrol decreased the IL-1beta-stimulated phosphorylation degree of IkappaBalpha and P65. celastrol 10-19 NFKB inhibitor alpha Rattus norvegicus 80-92 32112120-10 2020 Moreover, celastrol decreased the IL-1beta-stimulated phosphorylation degree of IkappaBalpha and P65. celastrol 10-19 synaptotagmin 1 Rattus norvegicus 97-100 31904241-0 2020 Celastrol-loaded galactosylated liposomes effectively inhibit AKT/c-Met-triggered rapid hepatocarcinogenesis in mice. celastrol 0-9 met proto-oncogene Mus musculus 66-71 31982489-0 2020 SERCA and P-glycoprotein inhibition and ATP depletion are necessary for celastrol-induced autophagic cell death and collateral sensitivity in multidrug-resistant tumor cells. celastrol 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 10-24 31982489-6 2020 Here, we unraveled SERCA and P-gp as double targets of the triterpenoid, celastrol to reverse MDR. celastrol 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 31982489-7 2020 Celastrol inhibited both SERCA and P-gp to stimulate calcium-mediated autophagy and ATP depletion, thereby induced collateral sensitivity in MDR cancer cells. celastrol 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 31841695-0 2020 Preventive effects of "ovalbumin-conjugated celastrol-loaded nanomicelles"" in a mouse model of ovalbumin-induced allergic airway inflammation. celastrol 44-53 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 23-32 32110017-1 2020 Background: Celastrol (CEL), a triterpene extracted from the Chinese herb tripterygium wilfordii, has been reported to have profound anticancer activities. celastrol 12-21 carboxyl ester lipase Mus musculus 23-26 31841695-0 2020 Preventive effects of "ovalbumin-conjugated celastrol-loaded nanomicelles"" in a mouse model of ovalbumin-induced allergic airway inflammation. celastrol 44-53 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 96-105 31841695-3 2020 We constructed ovalbumin (OVA)-conjugated celastrol-loaded nanomicelles (OVA-NMs-celastrol), wherein celastrol (a bioactive anti-inflammatory compound) was loaded into carboxyl-functioned polymeric nanomicelles using a thin-film hydration method. celastrol 42-51 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 15-24 31841695-3 2020 We constructed ovalbumin (OVA)-conjugated celastrol-loaded nanomicelles (OVA-NMs-celastrol), wherein celastrol (a bioactive anti-inflammatory compound) was loaded into carboxyl-functioned polymeric nanomicelles using a thin-film hydration method. celastrol 81-90 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 15-24 31841695-3 2020 We constructed ovalbumin (OVA)-conjugated celastrol-loaded nanomicelles (OVA-NMs-celastrol), wherein celastrol (a bioactive anti-inflammatory compound) was loaded into carboxyl-functioned polymeric nanomicelles using a thin-film hydration method. celastrol 81-90 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 15-24 31841695-8 2020 Further, in vivo results showed that treatment with OVA-NMs-celastrol could decrease OVA specific IgE and histamine levels, Th2 cytokine (IL-4, IL-5) levels, and inflammatory cell infiltration in the lung tissues. celastrol 60-69 heart and neural crest derivatives expressed 2 Mus musculus 124-127 31841695-8 2020 Further, in vivo results showed that treatment with OVA-NMs-celastrol could decrease OVA specific IgE and histamine levels, Th2 cytokine (IL-4, IL-5) levels, and inflammatory cell infiltration in the lung tissues. celastrol 60-69 interleukin 4 Mus musculus 138-142 31841695-8 2020 Further, in vivo results showed that treatment with OVA-NMs-celastrol could decrease OVA specific IgE and histamine levels, Th2 cytokine (IL-4, IL-5) levels, and inflammatory cell infiltration in the lung tissues. celastrol 60-69 interleukin 5 Mus musculus 144-148 32041250-6 2020 Moreover, inflammatory responses induced by gamma irradiation, as demonstrated by increased levels of IL-6, TNF-alpha, and IL-1beta, were also blocked by celastrol. celastrol 154-163 interleukin 6 Homo sapiens 102-106 32041250-6 2020 Moreover, inflammatory responses induced by gamma irradiation, as demonstrated by increased levels of IL-6, TNF-alpha, and IL-1beta, were also blocked by celastrol. celastrol 154-163 tumor necrosis factor Homo sapiens 108-117 32041250-6 2020 Moreover, inflammatory responses induced by gamma irradiation, as demonstrated by increased levels of IL-6, TNF-alpha, and IL-1beta, were also blocked by celastrol. celastrol 154-163 interleukin 1 alpha Homo sapiens 123-131 32041250-7 2020 The increased activity of NF-kappaB DNA binding following gamma radiation was significantly attenuated after celastrol treatment. celastrol 109-118 nuclear factor kappa B subunit 1 Homo sapiens 26-35 32116702-0 2020 Celastrol Suppresses Glioma Vasculogenic Mimicry Formation and Angiogenesis by Blocking the PI3K/Akt/mTOR Signaling Pathway. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 97-100 32116702-0 2020 Celastrol Suppresses Glioma Vasculogenic Mimicry Formation and Angiogenesis by Blocking the PI3K/Akt/mTOR Signaling Pathway. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 101-105 32116702-6 2020 Periodic acid Schiff (PAS)-CD31 staining revealed that celastrol inhibited both VM and angiogenesis in tumor tissues. celastrol 55-64 platelet and endothelial cell adhesion molecule 1 Homo sapiens 27-31 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 platelet and endothelial cell adhesion molecule 1 Homo sapiens 91-95 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 kinase insert domain receptor Homo sapiens 97-140 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 kinase insert domain receptor Homo sapiens 142-147 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 angiopoietin 2 Homo sapiens 152-172 32041250-8 2020 In the irradiated mice, treatment with celastrol significantly improved overall survival rate, reduced the excessive inflammatory responses, and decreased NF-kappaB activity. celastrol 39-48 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 155-164 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 vascular endothelial growth factor A Homo sapiens 177-182 32041250-9 2020 As a NF-kappaB pathway blocker and antioxidant, celastrol may represent a promising pharmacological agent with protective effects against gamma irradiation-induced injury. celastrol 48-57 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 5-14 31989218-0 2020 Novel complementary antitumour effects of celastrol and metformin by targeting IkappaBkappaB, apoptosis and NLRP3 inflammasome activation in diethylnitrosamine-induced murine hepatocarcinogenesis. celastrol 42-51 NLR family, pyrin domain containing 3 Mus musculus 108-113 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 EPH receptor A2 Homo sapiens 228-235 32116702-7 2020 Additionally, celastrol reduced the expression levels of the angiogenesis-related proteins CD31, vascular endothelial growth factor receptor (VEGFR) 2, angiopoietin (Ang) 2 and VEGFA, VM-related proteins ephrin type-A receptor (EphA) 2, and vascular endothelial (VE)-cadherin. celastrol 14-23 cadherin 5 Homo sapiens 241-275 32116702-8 2020 Hypoxia inducible factor (HIF)-1alpha, phosphorylated PI3K, Akt, and mTOR were also downregulated by treatment with celastrol. celastrol 116-125 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-37 32116702-8 2020 Hypoxia inducible factor (HIF)-1alpha, phosphorylated PI3K, Akt, and mTOR were also downregulated by treatment with celastrol. celastrol 116-125 thymoma viral proto-oncogene 1 Mus musculus 60-63 32116702-8 2020 Hypoxia inducible factor (HIF)-1alpha, phosphorylated PI3K, Akt, and mTOR were also downregulated by treatment with celastrol. celastrol 116-125 mechanistic target of rapamycin kinase Mus musculus 69-73 32116702-9 2020 In vitro, we further demonstrated that celastrol inhibited the growth, migration, and invasion of U87 and U251 cells, disrupted VM formation, and blocked the activity of PI3K, Akt, and mTOR. celastrol 39-48 AKT serine/threonine kinase 1 Homo sapiens 176-179 32116702-9 2020 In vitro, we further demonstrated that celastrol inhibited the growth, migration, and invasion of U87 and U251 cells, disrupted VM formation, and blocked the activity of PI3K, Akt, and mTOR. celastrol 39-48 mechanistic target of rapamycin kinase Homo sapiens 185-189 32116702-10 2020 Collectively, our data suggest that celastrol inhibits VM formation and angiogenesis likely by regulating the PI3K/Akt/mTOR signaling pathway. celastrol 36-45 AKT serine/threonine kinase 1 Homo sapiens 115-118 32116702-10 2020 Collectively, our data suggest that celastrol inhibits VM formation and angiogenesis likely by regulating the PI3K/Akt/mTOR signaling pathway. celastrol 36-45 mechanistic target of rapamycin kinase Homo sapiens 119-123 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 20-29 caspase 9 Mus musculus 138-147 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 20-29 BCL2-associated X protein Mus musculus 173-176 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 20-29 B cell leukemia/lymphoma 2 Mus musculus 177-182 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 34-43 caspase 9 Mus musculus 138-147 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 34-43 caspase 3 Mus musculus 152-161 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 34-43 BCL2-associated X protein Mus musculus 173-176 31989218-8 2020 In contrast, in the celastrol and celastrol + metformin groups, the apoptotic potential was amplified, as revealed by the increase in the caspase-9 and caspase-3 levels and Bax:BCL-2 ratio. celastrol 34-43 B cell leukemia/lymphoma 2 Mus musculus 177-182 31989218-9 2020 In addition to their repressive effect on the gene expression of NFkappaBp65, TNFR and TLR4, metformin and celastrol inhibited phosphorylation-induced activation of IkappaBkappaB and NFkappaBp65 and decreased IkappaBalpha degradation. celastrol 107-116 tumor necrosis factor receptor superfamily, member 1a Mus musculus 78-82 31989218-9 2020 In addition to their repressive effect on the gene expression of NFkappaBp65, TNFR and TLR4, metformin and celastrol inhibited phosphorylation-induced activation of IkappaBkappaB and NFkappaBp65 and decreased IkappaBalpha degradation. celastrol 107-116 toll-like receptor 4 Mus musculus 87-91 31989218-9 2020 In addition to their repressive effect on the gene expression of NFkappaBp65, TNFR and TLR4, metformin and celastrol inhibited phosphorylation-induced activation of IkappaBkappaB and NFkappaBp65 and decreased IkappaBalpha degradation. celastrol 107-116 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 209-221 31989218-10 2020 Combination therapy with metformin and celastrol repressed markers of angiogenesis, metastasis and tumour proliferation, as revealed by the decreased hepatic levels of VEGF, MMP-2/9 and cyclin D1 mRNA, respectively. celastrol 39-48 vascular endothelial growth factor A Mus musculus 168-172 31989218-10 2020 Combination therapy with metformin and celastrol repressed markers of angiogenesis, metastasis and tumour proliferation, as revealed by the decreased hepatic levels of VEGF, MMP-2/9 and cyclin D1 mRNA, respectively. celastrol 39-48 matrix metallopeptidase 2 Mus musculus 174-181 31989218-10 2020 Combination therapy with metformin and celastrol repressed markers of angiogenesis, metastasis and tumour proliferation, as revealed by the decreased hepatic levels of VEGF, MMP-2/9 and cyclin D1 mRNA, respectively. celastrol 39-48 cyclin D1 Mus musculus 186-195 31989218-11 2020 In conclusion, by inhibiting NLRP3 inflammasome and its prerequisite NFkappaB signalling, simultaneous administration of metformin and celastrol appears to have additive benefits in the treatment of HCC compared to cela monotherapy. celastrol 135-144 NLR family, pyrin domain containing 3 Mus musculus 29-34 31989218-11 2020 In conclusion, by inhibiting NLRP3 inflammasome and its prerequisite NFkappaB signalling, simultaneous administration of metformin and celastrol appears to have additive benefits in the treatment of HCC compared to cela monotherapy. celastrol 135-144 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 69-77 31949255-13 2020 We are the first to identify the involvement of a cysteine metabolism/reactive oxygen species/p53/Bax/caspase 9/caspase 3 pathway in celastrol-triggered mitochondrial apoptosis in HL-60 and NB-4 cells, providing a novel underlying mechanism through which celastrol could be used to treat acute myeloid leukaemia, especially acute promyelocytic leukaemia. celastrol 133-142 tumor protein p53 Homo sapiens 94-97 31901889-0 2020 Celastrol is a novel selective agonist of cannabinoid receptor 2 with anti-inflammatory and anti-fibrotic activity in a mouse model of systemic sclerosis. celastrol 0-9 cannabinoid receptor 2 (macrophage) Mus musculus 42-64 31901889-8 2020 RESULTS: Celastrol was identified as a new agonist of CB2 by using SLCA. celastrol 9-18 cannabinoid receptor 2 (macrophage) Mus musculus 54-57 31901889-9 2020 Furthermore, celastrol triggers several CB2-mediated downstream signaling pathways, including calcium mobilization, inhibition of cAMP accumulation, and receptor desensitization in a dose-dependent manner, and it has a moderate selectivity on CB1. celastrol 13-22 cannabinoid receptor 2 (macrophage) Mus musculus 40-43 31901889-9 2020 Furthermore, celastrol triggers several CB2-mediated downstream signaling pathways, including calcium mobilization, inhibition of cAMP accumulation, and receptor desensitization in a dose-dependent manner, and it has a moderate selectivity on CB1. celastrol 13-22 cannabinoid receptor 1 (brain) Mus musculus 243-246 31901889-12 2020 CONCLUSION: Taken together, celastrol is identified a novel selective CB2 agonist using a new developed arrestin-based SLCA, and CB2 activation by celastrol reduces the inflammatory response, and prevents the development of dermal fibrosis in bleomycin-induced systemic sclerosis mouse model. celastrol 28-37 cannabinoid receptor 2 (macrophage) Mus musculus 70-73 31901889-12 2020 CONCLUSION: Taken together, celastrol is identified a novel selective CB2 agonist using a new developed arrestin-based SLCA, and CB2 activation by celastrol reduces the inflammatory response, and prevents the development of dermal fibrosis in bleomycin-induced systemic sclerosis mouse model. celastrol 147-156 cannabinoid receptor 2 (macrophage) Mus musculus 129-132 31949255-13 2020 We are the first to identify the involvement of a cysteine metabolism/reactive oxygen species/p53/Bax/caspase 9/caspase 3 pathway in celastrol-triggered mitochondrial apoptosis in HL-60 and NB-4 cells, providing a novel underlying mechanism through which celastrol could be used to treat acute myeloid leukaemia, especially acute promyelocytic leukaemia. celastrol 133-142 BCL2 associated X, apoptosis regulator Homo sapiens 98-101 31949255-13 2020 We are the first to identify the involvement of a cysteine metabolism/reactive oxygen species/p53/Bax/caspase 9/caspase 3 pathway in celastrol-triggered mitochondrial apoptosis in HL-60 and NB-4 cells, providing a novel underlying mechanism through which celastrol could be used to treat acute myeloid leukaemia, especially acute promyelocytic leukaemia. celastrol 133-142 caspase 9 Homo sapiens 102-111 31949255-13 2020 We are the first to identify the involvement of a cysteine metabolism/reactive oxygen species/p53/Bax/caspase 9/caspase 3 pathway in celastrol-triggered mitochondrial apoptosis in HL-60 and NB-4 cells, providing a novel underlying mechanism through which celastrol could be used to treat acute myeloid leukaemia, especially acute promyelocytic leukaemia. celastrol 133-142 caspase 3 Homo sapiens 112-121 31957323-0 2020 Antitumor activity of celastrol by inhibition of proliferation, invasion, and migration in cholangiocarcinoma via PTEN/PI3K/Akt pathway. celastrol 22-31 thymoma viral proto-oncogene 1 Mus musculus 124-127 31957323-8 2020 To further find the mechanism involved in the celastrol-induced biological functions, LY204002, a PI3K/Akt signaling inhibitor, and an Akt-1 overexpression plasmid were employed to find whether PI3K/Akt pathway was involved in the celastrol-induced CCA cell inhibition. celastrol 46-55 thymoma viral proto-oncogene 1 Mus musculus 103-106 31957323-8 2020 To further find the mechanism involved in the celastrol-induced biological functions, LY204002, a PI3K/Akt signaling inhibitor, and an Akt-1 overexpression plasmid were employed to find whether PI3K/Akt pathway was involved in the celastrol-induced CCA cell inhibition. celastrol 46-55 thymoma viral proto-oncogene 1 Mus musculus 135-140 31957323-8 2020 To further find the mechanism involved in the celastrol-induced biological functions, LY204002, a PI3K/Akt signaling inhibitor, and an Akt-1 overexpression plasmid were employed to find whether PI3K/Akt pathway was involved in the celastrol-induced CCA cell inhibition. celastrol 46-55 thymoma viral proto-oncogene 1 Mus musculus 135-138 31957323-9 2020 Additionally, short interfering RNA (siRNA) was also used to investigate the mechanism involved in the celastrol-induced PI3K/Akt signaling inhibition. celastrol 103-112 thymoma viral proto-oncogene 1 Mus musculus 126-129 31957323-13 2020 Further mechanistic study identified that celastrol regulated the PI3K/Akt signaling pathway, and the antitumor efficacy was likely due to the upregulation of PTEN, a negative regulator of PI3K/Akt. celastrol 42-51 thymoma viral proto-oncogene 1 Mus musculus 71-74 31957323-13 2020 Further mechanistic study identified that celastrol regulated the PI3K/Akt signaling pathway, and the antitumor efficacy was likely due to the upregulation of PTEN, a negative regulator of PI3K/Akt. celastrol 42-51 phosphatase and tensin homolog Mus musculus 159-163 31957323-13 2020 Further mechanistic study identified that celastrol regulated the PI3K/Akt signaling pathway, and the antitumor efficacy was likely due to the upregulation of PTEN, a negative regulator of PI3K/Akt. celastrol 42-51 thymoma viral proto-oncogene 1 Mus musculus 194-197 31957323-14 2020 Blockage of PTEN abolished the celastrol-induced PI3K/Akt signaling inhibition. celastrol 31-40 phosphatase and tensin homolog Mus musculus 12-16 31957323-14 2020 Blockage of PTEN abolished the celastrol-induced PI3K/Akt signaling inhibition. celastrol 31-40 thymoma viral proto-oncogene 1 Mus musculus 54-57 31957323-16 2020 CONCLUSIONS: Overall, our study elucidated a mechanistic framework for the anti-CCA effects of celastrol via PTEN/PI3K/Akt pathway. celastrol 95-104 phosphatase and tensin homolog Mus musculus 109-113 31957323-16 2020 CONCLUSIONS: Overall, our study elucidated a mechanistic framework for the anti-CCA effects of celastrol via PTEN/PI3K/Akt pathway. celastrol 95-104 thymoma viral proto-oncogene 1 Mus musculus 119-122 31742890-0 2020 Celastrol exerts anti-inflammatory effect in liver fibrosis via activation of AMPK-SIRT3 signalling. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 78-82 31742890-11 2020 We further found that depletion of AMPK significantly attenuated the inhibitory effect of celastrol on inflammation. celastrol 90-99 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 35-39 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 14-23 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31742890-0 2020 Celastrol exerts anti-inflammatory effect in liver fibrosis via activation of AMPK-SIRT3 signalling. celastrol 0-9 sirtuin 3 Homo sapiens 83-88 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 14-23 sirtuin 3 Homo sapiens 111-116 31742890-3 2020 This study was to investigate the anti-inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol-induced anti-inflammatory effects with a focus on AMPK-SIRT3 signalling. celastrol 126-135 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 186-190 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 141-150 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 106-110 31742890-12 2020 Collectively, celastrol attenuated liver fibrosis mainly through inhibition of inflammation by activating AMPK-SIRT3 signalling, which makes celastrol be a potential candidate compound in treating or protecting against liver fibrosis. celastrol 141-150 sirtuin 3 Homo sapiens 111-116 31742890-3 2020 This study was to investigate the anti-inflammatory effect of celastrol in liver fibrosis and to further reveal mechanisms of celastrol-induced anti-inflammatory effects with a focus on AMPK-SIRT3 signalling. celastrol 126-135 sirtuin 3 Homo sapiens 191-196 31742890-6 2020 Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. celastrol 15-24 sirtuin 3 Homo sapiens 35-40 31742890-6 2020 Interestingly, celastrol increased SIRT3 promoter activity and SIRT3 expression both in fibrotic liver and in activated HSCs. celastrol 15-24 sirtuin 3 Homo sapiens 63-68 31742890-7 2020 Furthermore, SIRT3 silencing evidently ameliorated the anti-inflammatory potential of celastrol. celastrol 86-95 sirtuin 3 Homo sapiens 13-18 31742890-8 2020 Besides, we found that celastrol could increase the AMPK phosphorylation. celastrol 23-32 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 52-56 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 beclin 1, autophagy related Mus musculus 68-76 31734262-5 2020 RESULTS: The results suggest that celastrol acts against SLE by regulating the function of several signaling proteins, such as interleukin 10, tumor necrosis factor, and matrix metalloprotein 9, which regulate signaling pathways involving mitogen-activated protein kinase and tumor necrosis factor as well as apoptosis pathways. celastrol 34-43 interleukin 10 Homo sapiens 127-141 31734262-5 2020 RESULTS: The results suggest that celastrol acts against SLE by regulating the function of several signaling proteins, such as interleukin 10, tumor necrosis factor, and matrix metalloprotein 9, which regulate signaling pathways involving mitogen-activated protein kinase and tumor necrosis factor as well as apoptosis pathways. celastrol 34-43 tumor necrosis factor Homo sapiens 143-193 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 autophagy/beclin 1 regulator 1 Mus musculus 79-85 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 phosphatidylinositol 3-kinase catalytic subunit type 3 Mus musculus 88-93 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 autophagy related 7 Mus musculus 96-100 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 autophagy related 12 Mus musculus 103-108 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 PTEN induced putative kinase 1 Mus musculus 140-145 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 Parkinson disease (autosomal recessive, early onset) 7 Mus musculus 148-152 31906147-8 2019 In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1 , Ambra1 , Vps34 , Atg7 , Atg12 , and LC3-II ), and mitophagy (PINK1 , DJ-1 , and LRRK2 ), and these might be associated with MPAK signaling pathways. celastrol 12-21 leucine-rich repeat kinase 2 Mus musculus 159-164 31906147-10 2019 In the PD mouse model, celastrol suppresses motor symptoms and neurodegeneration in the substantia nigra and striatum and enhances mitophagy (PINK1 and DJ-1 ) in the striatum. celastrol 23-32 PTEN induced putative kinase 1 Mus musculus 142-147 31906147-10 2019 In the PD mouse model, celastrol suppresses motor symptoms and neurodegeneration in the substantia nigra and striatum and enhances mitophagy (PINK1 and DJ-1 ) in the striatum. celastrol 23-32 Parkinson disease (autosomal recessive, early onset) 7 Mus musculus 153-157 31725288-0 2019 Discovery of novel celastrol derivatives as Hsp90-Cdc37 interaction disruptors with antitumour activity. celastrol 19-28 heat shock protein 90 alpha family class A member 1 Homo sapiens 44-49 32043019-0 2020 Celastrol Alleviates Aortic Valve Calcification Via Inhibition of NADPH Oxidase 2 in Valvular Interstitial Cells. celastrol 0-9 cytochrome b-245 heavy chain Oryctolagus cuniculus 66-81 32043019-9 2020 Mechanistically, either celastrol treatment or knockdown of Nox2 significantly inhibited glycogen synthase kinase 3 beta/beta-catenin signaling, leading to attenuation of fibrogenic and osteogenic responses of AVICs. celastrol 24-33 glycogen synthase kinase-3 beta Oryctolagus cuniculus 89-120 32043019-9 2020 Mechanistically, either celastrol treatment or knockdown of Nox2 significantly inhibited glycogen synthase kinase 3 beta/beta-catenin signaling, leading to attenuation of fibrogenic and osteogenic responses of AVICs. celastrol 24-33 catenin alpha-1 Oryctolagus cuniculus 121-133 32043019-12 2020 Celastrol is effective to alleviate CAVD, likely through the inhibition of Nox2-mediated glycogen synthase kinase 3 beta/beta-catenin pathway in AVICs. celastrol 0-9 cytochrome b-245 heavy chain Oryctolagus cuniculus 75-79 32043019-12 2020 Celastrol is effective to alleviate CAVD, likely through the inhibition of Nox2-mediated glycogen synthase kinase 3 beta/beta-catenin pathway in AVICs. celastrol 0-9 glycogen synthase kinase-3 beta Oryctolagus cuniculus 89-120 32043019-12 2020 Celastrol is effective to alleviate CAVD, likely through the inhibition of Nox2-mediated glycogen synthase kinase 3 beta/beta-catenin pathway in AVICs. celastrol 0-9 catenin alpha-1 Oryctolagus cuniculus 121-133 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 175-178 heat shock protein 90 alpha family class A member 1 Homo sapiens 77-82 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 175-178 cell division cycle 37, HSP90 cochaperone Homo sapiens 83-88 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 201-204 heat shock protein 90 alpha family class A member 1 Homo sapiens 77-82 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 201-204 cell division cycle 37, HSP90 cochaperone Homo sapiens 83-88 31725288-0 2019 Discovery of novel celastrol derivatives as Hsp90-Cdc37 interaction disruptors with antitumour activity. celastrol 19-28 cell division cycle 37, HSP90 cochaperone Homo sapiens 50-55 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 164-173 heat shock protein 90 alpha family class A member 1 Homo sapiens 77-82 31725288-3 2019 The capability to disrupt the Hsp90-Cdc37 interaction was stronger than that of CEL. celastrol 80-83 heat shock protein 90 alpha family class A member 1 Homo sapiens 30-35 31725288-3 2019 The capability to disrupt the Hsp90-Cdc37 interaction was stronger than that of CEL. celastrol 80-83 cell division cycle 37, HSP90 cochaperone Homo sapiens 36-41 31725288-1 2019 To develop novel and efficient heat shock protein 90-cell division cycle 37 (Hsp90-Cdc37) interaction disruptors, several lipophilic fragments were introduced into celastrol (CEL) to synthesize 48 new CEL derivatives. celastrol 164-173 cell division cycle 37, HSP90 cochaperone Homo sapiens 83-88 31694174-0 2019 Early Celastrol Administration Prevents Ketamine-Induced Psychotic-Like Behavioral Dysfunctions, Oxidative Stress and IL-10 Reduction in The Cerebellum of Adult Mice. celastrol 6-15 interleukin 10 Mus musculus 118-123 31663764-0 2019 Transferrin-Functionalized Microemulsions Coloaded with Coix Seed Oil and Tripterine Deeply Penetrate To Improve Cervical Cancer Therapy. celastrol 74-84 transferrin Mus musculus 0-11 31663764-2 2019 In this study, we showed that coix seed oil and tripterine coloaded microemulsions with a transferrin modification (Tf-CT-MEs) could improve the treatment of cervical cancer. celastrol 48-58 transferrin Mus musculus 90-101 31694174-16 2019 While no changes were observed for IL-6 and IL-1beta levels, ketamine determined a reduction of cerebellar IL-10 expression, which was prevented by early celastrol treatment. celastrol 154-163 interleukin 10 Mus musculus 107-112 31735550-0 2019 Celastrol-induced degradation of FANCD2 sensitizes pediatric high-grade gliomas to the DNA-crosslinking agent carboplatin. celastrol 0-9 FA complementation group D2 Homo sapiens 33-39 31735550-5 2019 METHODS: We determined the capacity of celastrol, a BBB-penetrable compound that degrades FANCD2, to sensitize glioma cells to the archetypical DNA-crosslinking agent carboplatin in vitro in seven patient-derived pHGG models. celastrol 39-48 FA complementation group D2 Homo sapiens 90-96 31735550-8 2019 FINDINGS: FANCD2 is overexpressed in HGGs and depletion of FANCD2 by celastrol synergises with carboplatin to induce cytotoxicity. celastrol 69-78 FA complementation group D2 Homo sapiens 59-65 31735550-10 2019 In addition, our results suggest that celastrol treatment stalls ongoing replication forks, causing sensitivity to DNA-crosslinking in FANCD2-dependent glioma cells. celastrol 38-47 FA complementation group D2 Homo sapiens 135-141 31739592-0 2019 Celastrol Induces Necroptosis and Ameliorates Inflammation via Targeting Biglycan in Human Gastric Carcinoma. celastrol 0-9 biglycan Homo sapiens 73-81 31739592-5 2019 More importantly, celastrol down-regulated biglycan (BGN) protein, which is critical for gastric cancer migration and invasion. celastrol 18-27 biglycan Homo sapiens 43-51 31739592-5 2019 More importantly, celastrol down-regulated biglycan (BGN) protein, which is critical for gastric cancer migration and invasion. celastrol 18-27 biglycan Homo sapiens 53-56 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 receptor interacting serine/threonine kinase 1 Homo sapiens 33-69 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 receptor interacting serine/threonine kinase 1 Homo sapiens 71-75 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 receptor interacting serine/threonine kinase 3 Homo sapiens 80-84 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 mixed lineage kinase domain like pseudokinase Homo sapiens 131-163 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 mixed lineage kinase domain like pseudokinase Homo sapiens 165-169 31739592-6 2019 Furthermore, celastrol activated receptor-interacting protein 1 and 3 (RIP1 and RIP3) and subsequently promoted the translation of mixed-lineage kinase domain-like (MLKL) from cytoplasm to plasma membrane, leading to necroptosis of gastric cancer cell, which was blocked by over-expression BGN. celastrol 13-22 biglycan Homo sapiens 290-293 31739592-7 2019 In addition, celastrol suppressed the release of pro-inflammatory cytokines TNF-alpha and IL-8 in HGC27 and AGS cells, which was reversed by over-expression BGN. celastrol 13-22 tumor necrosis factor Homo sapiens 76-85 31739592-7 2019 In addition, celastrol suppressed the release of pro-inflammatory cytokines TNF-alpha and IL-8 in HGC27 and AGS cells, which was reversed by over-expression BGN. celastrol 13-22 C-X-C motif chemokine ligand 8 Homo sapiens 90-94 31739592-7 2019 In addition, celastrol suppressed the release of pro-inflammatory cytokines TNF-alpha and IL-8 in HGC27 and AGS cells, which was reversed by over-expression BGN. celastrol 13-22 biglycan Homo sapiens 157-160 31739592-8 2019 Taken together, we identified celastrol as a necroptosis inducer, activated RIP1/RIP3/MLKL pathway and suppressed the level of pro-inflammatory cytokines by down-regulating BGN in HGC-27 and AGS cells, which supported the feasibility of celastrol in gastric cancer therapy. celastrol 30-39 receptor interacting serine/threonine kinase 1 Homo sapiens 76-80 31739592-8 2019 Taken together, we identified celastrol as a necroptosis inducer, activated RIP1/RIP3/MLKL pathway and suppressed the level of pro-inflammatory cytokines by down-regulating BGN in HGC-27 and AGS cells, which supported the feasibility of celastrol in gastric cancer therapy. celastrol 30-39 receptor interacting serine/threonine kinase 3 Homo sapiens 81-85 31739592-8 2019 Taken together, we identified celastrol as a necroptosis inducer, activated RIP1/RIP3/MLKL pathway and suppressed the level of pro-inflammatory cytokines by down-regulating BGN in HGC-27 and AGS cells, which supported the feasibility of celastrol in gastric cancer therapy. celastrol 30-39 mixed lineage kinase domain like pseudokinase Homo sapiens 86-90 31739592-8 2019 Taken together, we identified celastrol as a necroptosis inducer, activated RIP1/RIP3/MLKL pathway and suppressed the level of pro-inflammatory cytokines by down-regulating BGN in HGC-27 and AGS cells, which supported the feasibility of celastrol in gastric cancer therapy. celastrol 30-39 biglycan Homo sapiens 173-176 31694174-6 2019 Furthermore, celastrol effects on ketamine-induced alterations of proinflammatory (TNF-alpha, IL-6 and IL-1beta) and anti-inflammatory (IL-10) cytokines in this brain region were evaluated. celastrol 13-22 tumor necrosis factor Mus musculus 83-92 31694174-6 2019 Furthermore, celastrol effects on ketamine-induced alterations of proinflammatory (TNF-alpha, IL-6 and IL-1beta) and anti-inflammatory (IL-10) cytokines in this brain region were evaluated. celastrol 13-22 interleukin 6 Mus musculus 94-98 31694174-6 2019 Furthermore, celastrol effects on ketamine-induced alterations of proinflammatory (TNF-alpha, IL-6 and IL-1beta) and anti-inflammatory (IL-10) cytokines in this brain region were evaluated. celastrol 13-22 interleukin 1 alpha Mus musculus 103-111 31694174-6 2019 Furthermore, celastrol effects on ketamine-induced alterations of proinflammatory (TNF-alpha, IL-6 and IL-1beta) and anti-inflammatory (IL-10) cytokines in this brain region were evaluated. celastrol 13-22 interleukin 10 Mus musculus 136-141 31694174-11 2019 Celastrol per se induced NOX1 decrease in the cerebellum. celastrol 0-9 NADPH oxidase 1 Mus musculus 25-29 31637185-0 2019 Celastrol inhibits migration, proliferation and transforming growth factor-beta2-induced epithelial-mesenchymal transition in lens epithelial cells. celastrol 0-9 transforming growth factor beta 2 Homo sapiens 48-80 31635084-0 2019 Identification of Celastrol as a Novel YAP-TEAD Inhibitor for Cancer Therapy by High Throughput Screening with Ultrasensitive YAP/TAZ-TEAD Biosensors. celastrol 18-27 Yes1 associated transcriptional regulator Homo sapiens 39-42 31635084-0 2019 Identification of Celastrol as a Novel YAP-TEAD Inhibitor for Cancer Therapy by High Throughput Screening with Ultrasensitive YAP/TAZ-TEAD Biosensors. celastrol 18-27 Yes1 associated transcriptional regulator Homo sapiens 126-129 31635084-0 2019 Identification of Celastrol as a Novel YAP-TEAD Inhibitor for Cancer Therapy by High Throughput Screening with Ultrasensitive YAP/TAZ-TEAD Biosensors. celastrol 18-27 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 130-133 31635084-5 2019 Using this biosensor, we have performed an in vitro high throughput screen (HTS) of small molecule compounds and have identified and validated the drug Celastrol as a novel inhibitor of YAP/TAZ-TEAD interaction. celastrol 152-161 Yes1 associated transcriptional regulator Homo sapiens 186-189 31635084-5 2019 Using this biosensor, we have performed an in vitro high throughput screen (HTS) of small molecule compounds and have identified and validated the drug Celastrol as a novel inhibitor of YAP/TAZ-TEAD interaction. celastrol 152-161 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 190-193 31637185-2 2019 METHODS: Human LEC line SRA01/04 was treated with celastrol and transforming growth factor-beta2 (TGF-beta2). celastrol 50-59 C-C motif chemokine ligand 16 Homo sapiens 15-18 31637185-7 2019 Moreover, celastrol inhibited epithelial-mesenchymal transition (EMT) by the blockade of TGF-beta/Smad and Jagged/Notch signaling pathways. celastrol 10-19 transforming growth factor beta 2 Homo sapiens 89-97 31637185-8 2019 CONCLUSION: Our study demonstrates that celastrol could inhibit TGF-beta2-induced lens fibrosis and raises the possibility that celastrol could be a potential novel drug in prevention and treatment of fibrotic cataract. celastrol 40-49 transforming growth factor beta 2 Homo sapiens 64-73 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 interleukin 6 Mus musculus 120-124 31667381-4 2019 We further found that Celastrol, one of main components of TWHF, inhibits hERG with an IC50 of 0.83 muM. celastrol 22-31 ETS transcription factor ERG Homo sapiens 74-78 31667381-6 2019 Our data suggest that inhibition of hERG channel activity by Celastrol contributed to TWHF cardiotoxicity. celastrol 61-70 ETS transcription factor ERG Homo sapiens 36-40 31281953-0 2019 Celastrol enhances TRAIL-induced apoptosis in human glioblastoma via the death receptor pathway. celastrol 0-9 TNF superfamily member 10 Homo sapiens 19-24 31281953-4 2019 Celastrol is a pleiotropic compound from a traditional Chinese medicine that has proven to be useful as a sensitizer for TRAIL treatment. celastrol 0-9 TNF superfamily member 10 Homo sapiens 121-126 31281953-15 2019 Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP. celastrol 13-22 TNF receptor superfamily member 10b Homo sapiens 35-51 31281953-15 2019 Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP. celastrol 13-22 TNF receptor superfamily member 10b Homo sapiens 53-56 31281953-15 2019 Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP. celastrol 13-22 caspase 3 Homo sapiens 230-239 31281953-15 2019 Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP. celastrol 13-22 caspase 8 Homo sapiens 241-250 31281953-15 2019 Furthermore, celastrol upregulated death receptor 5 (DR5) at the mRNA and protein levels, and siRNA-mediated DR5 knockdown reduced the killing effect of the combination drug treatment on glioma cells and reduced the activation of caspase-3, caspase-8 and PARP. celastrol 13-22 poly(ADP-ribose) polymerase 1 Homo sapiens 255-259 31281953-16 2019 CONCLUSIONS: Taken together, the results of our study demonstrate that celastrol sensitizes glioma cells to TRAIL via the death receptor pathway and that DR5 plays an important role in the effects of this cotreatment. celastrol 71-80 TNF superfamily member 10 Homo sapiens 108-113 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 interleukin 1 beta Mus musculus 126-134 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 tumor necrosis factor Mus musculus 136-145 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 nitric oxide synthase 2, inducible Mus musculus 147-151 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 arginase, liver Mus musculus 255-260 31454532-7 2019 As for macrophage M1/M2 polarization in liver, nano-celastrol reduced the expression of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in a dose-dependent manner and marginally increased the expression of macrophage M2 biomarkers (e.g., Arg-1, IL-10). celastrol 52-61 interleukin 10 Mus musculus 262-267 31276975-4 2019 Then we validated our predictions of four candidate targets (IKK-beta, JNK, COX-2, MEK1) by performing docking studies with celastrol. celastrol 124-133 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 61-69 31488870-0 2019 Lipocalin 2 Does Not Play A Role in Celastrol-Mediated Reduction in Food Intake and Body Weight. celastrol 36-45 asparagine-linked glycosylation 3 (alpha-1,3-mannosyltransferase) Mus musculus 17-20 31488870-1 2019 Celastrol is a leptin-sensitizing agent with profound anti-obesity effects in diet-induced obese (DIO) mice. celastrol 0-9 leptin Mus musculus 15-21 31488870-2 2019 However, the genes and pathways that mediate celastrol-induced leptin sensitization have not been fully understood. celastrol 45-54 leptin Mus musculus 63-69 31488870-2 2019 However, the genes and pathways that mediate celastrol-induced leptin sensitization have not been fully understood. celastrol 45-54 asparagine-linked glycosylation 3 (alpha-1,3-mannosyltransferase) Mus musculus 89-92 31488870-3 2019 By comparing the hypothalamic transcriptomes of celastrol and vehicle-treated DIO mice, we identified lipocalin-2 (Lcn2) as the gene most strongly upregulated by celastrol. celastrol 162-171 lipocalin 2 Mus musculus 102-113 31488870-3 2019 By comparing the hypothalamic transcriptomes of celastrol and vehicle-treated DIO mice, we identified lipocalin-2 (Lcn2) as the gene most strongly upregulated by celastrol. celastrol 162-171 lipocalin 2 Mus musculus 115-119 31488870-5 2019 Celastrol increased LCN2 protein levels in hypothalamus, liver, fat, muscle, and bone marrow, as well as in the plasma. celastrol 0-9 lipocalin 2 Mus musculus 20-24 31315437-9 2019 Finally, pharmacological inhibition of inflammation in ECs by celastrol rescued overexpression of VWF in cells expressing ApoE4. celastrol 62-71 von Willebrand factor Homo sapiens 98-101 31315437-9 2019 Finally, pharmacological inhibition of inflammation in ECs by celastrol rescued overexpression of VWF in cells expressing ApoE4. celastrol 62-71 apolipoprotein E Homo sapiens 122-127 31132532-0 2019 SAR study of celastrol analogs targeting Nur77-mediated inflammatory pathway. celastrol 13-22 sarcosine dehydrogenase Homo sapiens 0-3 31132532-0 2019 SAR study of celastrol analogs targeting Nur77-mediated inflammatory pathway. celastrol 13-22 nuclear receptor subfamily 4 group A member 1 Homo sapiens 41-46 31132532-2 2019 Our previous work found that celastrol, a pentacyclic triterpene, bound to Nur77 to inhibit inflammation in a Nur77-dependent manner. celastrol 29-38 nuclear receptor subfamily 4 group A member 1 Homo sapiens 75-80 31132532-2 2019 Our previous work found that celastrol, a pentacyclic triterpene, bound to Nur77 to inhibit inflammation in a Nur77-dependent manner. celastrol 29-38 nuclear receptor subfamily 4 group A member 1 Homo sapiens 110-115 31132532-3 2019 Celastrol binding to Nur77 promotes Nur77 translocation from nucleus to cytoplasm, resulting in clearance of inflamed mitochondria and then alleviation of inflammation. celastrol 0-9 nuclear receptor subfamily 4 group A member 1 Homo sapiens 21-26 31132532-3 2019 Celastrol binding to Nur77 promotes Nur77 translocation from nucleus to cytoplasm, resulting in clearance of inflamed mitochondria and then alleviation of inflammation. celastrol 0-9 nuclear receptor subfamily 4 group A member 1 Homo sapiens 36-41 31132532-4 2019 Here, we report the design, synthesis, SAR study and biological evaluation of a series of celastrol analogs. celastrol 90-99 sarcosine dehydrogenase Homo sapiens 39-42 31276975-4 2019 Then we validated our predictions of four candidate targets (IKK-beta, JNK, COX-2, MEK1) by performing docking studies with celastrol. celastrol 124-133 mitogen-activated protein kinase 8 Homo sapiens 71-74 31276975-4 2019 Then we validated our predictions of four candidate targets (IKK-beta, JNK, COX-2, MEK1) by performing docking studies with celastrol. celastrol 124-133 mitochondrially encoded cytochrome c oxidase II Homo sapiens 76-81 31276975-4 2019 Then we validated our predictions of four candidate targets (IKK-beta, JNK, COX-2, MEK1) by performing docking studies with celastrol. celastrol 124-133 mitogen-activated protein kinase kinase 1 Homo sapiens 83-87 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 matrix metallopeptidase 9 Homo sapiens 137-142 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 mitochondrially encoded cytochrome c oxidase II Homo sapiens 144-149 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 MYC proto-oncogene, bHLH transcription factor Homo sapiens 151-156 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 transforming growth factor beta 1 Homo sapiens 158-166 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 168-173 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 Janus kinase 1 Homo sapiens 175-180 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 Janus kinase 3 Homo sapiens 182-187 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 189-197 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 spleen associated tyrosine kinase Homo sapiens 199-202 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 matrix metallopeptidase 3 Homo sapiens 204-209 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 mitogen-activated protein kinase 8 Homo sapiens 211-214 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 mitogen-activated protein kinase kinase 1 Homo sapiens 219-223 31276975-5 2019 The results suggest that celastrol acts against rheumatoid arthritis by regulating the function of several signaling proteins, including MMP-9, COX-2, c-Myc, TGF-beta, c-JUN, JAK-1, JAK-3, IKK-beta, SYK, MMP-3, JNK and MEK1, which regulate the functions of Th1 and Th2 cells, macrophages, fibroblasts and endothelial cells in rheumatoid arthritis. celastrol 25-34 negative elongation factor complex member C/D Homo sapiens 257-260 31124139-0 2019 Ca2+ signalling plays a role in celastrol-mediated suppression of synovial fibroblasts of rheumatoid arthritis patients and experimental arthritis in rats. celastrol 32-41 carbonic anhydrase 2 Homo sapiens 0-3 31439870-9 2019 In addition, treatment with celastrol, an inhibitor of NLRP3 inflammasome, reduced the potency of macrophages to stimulate migration and invasion of melanoma cells. celastrol 28-37 NLR family, pyrin domain containing 3 Mus musculus 55-60 31485297-7 2019 We found that celastrol, at higher concentrations (above 1 muM), significantly increased ROS amount in LOVO/DX cells at both cytoplasmic and mitochondrial levels. celastrol 14-23 latexin Homo sapiens 59-62 31124139-1 2019 BACKGROUND AND PURPOSE: Celastrol exhibits anti-arthritic effects in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca2+ mobilization in treatment of RA remains undefined. celastrol 112-121 carbonic anhydrase 2 Rattus norvegicus 131-134 31124139-2 2019 Here, we describe a regulatory role for celastrol-induced Ca2+ signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. celastrol 40-49 carbonic anhydrase 2 Homo sapiens 58-61 31124139-7 2019 KEY RESULTS: Celastrol inhibited SERCA to induce autophagy-dependent cytotoxicity in RASFs/RAFLS via Ca2+ /calmodulin-dependent kinase kinase-beta-AMP-activated protein kinase-mTOR pathway and repressed arthritis symptoms in AIA rats. celastrol 13-22 carbonic anhydrase 2 Rattus norvegicus 101-104 31124139-7 2019 KEY RESULTS: Celastrol inhibited SERCA to induce autophagy-dependent cytotoxicity in RASFs/RAFLS via Ca2+ /calmodulin-dependent kinase kinase-beta-AMP-activated protein kinase-mTOR pathway and repressed arthritis symptoms in AIA rats. celastrol 13-22 mechanistic target of rapamycin kinase Rattus norvegicus 176-180 31124139-10 2019 Knockdown of calmodulin, calpains, and calcineurin in RAFLS confirmed the role of Ca2+ in celastrol-regulated gene expression. celastrol 90-99 carbonic anhydrase 2 Rattus norvegicus 82-85 31124139-11 2019 CONCLUSION AND IMPLICATIONS: Celastrol triggered Ca2+ signalling to induce autophagic cell death in RASFs/RAFLS and ameliorated arthritis in AIA rats mediated by calcium-dependent/-binding proteins facilitating the exploitation of anti-arthritic drugs based on manipulation of Ca2+ signalling. celastrol 29-38 carbonic anhydrase 2 Rattus norvegicus 49-52 31124139-11 2019 CONCLUSION AND IMPLICATIONS: Celastrol triggered Ca2+ signalling to induce autophagic cell death in RASFs/RAFLS and ameliorated arthritis in AIA rats mediated by calcium-dependent/-binding proteins facilitating the exploitation of anti-arthritic drugs based on manipulation of Ca2+ signalling. celastrol 29-38 carbonic anhydrase 2 Rattus norvegicus 277-280 31588349-11 2019 Likewise, celastrol pretreatment improved the GR and CAT activities. celastrol 10-19 glutathione-disulfide reductase Rattus norvegicus 46-48 31588349-11 2019 Likewise, celastrol pretreatment improved the GR and CAT activities. celastrol 10-19 catalase Rattus norvegicus 53-56 31051401-3 2019 The mechanism of pharmacological research indicated that 29 possessed the ability to disrupt Hsp90-Cdc37 complex which was stronger than celastrol. celastrol 137-146 heat shock protein 90 alpha family class A member 1 Homo sapiens 93-98 31051401-3 2019 The mechanism of pharmacological research indicated that 29 possessed the ability to disrupt Hsp90-Cdc37 complex which was stronger than celastrol. celastrol 137-146 cell division cycle 37, HSP90 cochaperone Homo sapiens 99-104 31285857-0 2019 Celastrol attenuates ox-LDL-induced mesangial cell proliferation via suppressing NLRP3 inflammasome activation. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 81-86 31266528-0 2019 Correction to: Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 15-24 mitogen-activated protein kinase 8 Homo sapiens 70-73 31266528-0 2019 Correction to: Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 15-24 AKT serine/threonine kinase 1 Homo sapiens 78-81 31266528-0 2019 Correction to: Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 15-24 mechanistic target of rapamycin kinase Homo sapiens 82-86 31285857-8 2019 As expected, celastrol pretreatment strikingly inhibited NLRP3 inflammasome activation and MC proliferation triggered by ox-LDL. celastrol 13-22 NLR family pyrin domain containing 3 Homo sapiens 57-62 31285857-9 2019 In summary, celastrol potently blocked ox-LDL-induced MC proliferation, possibly by inhibiting NLRP3 inflammasome activation. celastrol 12-21 NLR family pyrin domain containing 3 Homo sapiens 95-100 30928629-4 2019 In the present study, we found that celastrol inhibited the caspase-like (beta1), trypsin-like (beta2) and chymotrypsin-like (beta5) proteasome activities of purified human 20S proteasomes, with half-maximal inhibitory concentration (IC50) values of 7.1, 6.3, and 9.3 mumol/L, respectively. celastrol 36-45 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 74-79 30986447-0 2019 Celastrol-type HSP90 modulators allow for potent cardioprotective effects. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 15-20 30986447-3 2019 We have previously shown that celastrol, an HSP90 modulator, achieves cardioprotection through activation of cytoprotective HSP"s and heme-oxygenase-1 (HO-1). celastrol 30-39 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 44-49 30986447-3 2019 We have previously shown that celastrol, an HSP90 modulator, achieves cardioprotection through activation of cytoprotective HSP"s and heme-oxygenase-1 (HO-1). celastrol 30-39 heme oxygenase 1 Rattus norvegicus 134-150 30986447-3 2019 We have previously shown that celastrol, an HSP90 modulator, achieves cardioprotection through activation of cytoprotective HSP"s and heme-oxygenase-1 (HO-1). celastrol 30-39 heme oxygenase 1 Rattus norvegicus 152-156 30986447-8 2019 KEY FINDINGS: From a variety of HSP90 modulator chemotypes, the celastrol family was most efficient in inducing cytoprotective HSP70 and HO-1 protein overexpression and cell survival in vitro. celastrol 64-73 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 32-37 30986447-8 2019 KEY FINDINGS: From a variety of HSP90 modulator chemotypes, the celastrol family was most efficient in inducing cytoprotective HSP70 and HO-1 protein overexpression and cell survival in vitro. celastrol 64-73 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 127-132 30986447-8 2019 KEY FINDINGS: From a variety of HSP90 modulator chemotypes, the celastrol family was most efficient in inducing cytoprotective HSP70 and HO-1 protein overexpression and cell survival in vitro. celastrol 64-73 heme oxygenase 1 Rattus norvegicus 137-141 30986447-11 2019 SIGNIFICANCE: Celastrol backbone is essential for cardioprotection through HSP90 activity modulation. celastrol 14-23 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 75-80 30928629-4 2019 In the present study, we found that celastrol inhibited the caspase-like (beta1), trypsin-like (beta2) and chymotrypsin-like (beta5) proteasome activities of purified human 20S proteasomes, with half-maximal inhibitory concentration (IC50) values of 7.1, 6.3, and 9.3 mumol/L, respectively. celastrol 36-45 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 96-101 30928629-4 2019 In the present study, we found that celastrol inhibited the caspase-like (beta1), trypsin-like (beta2) and chymotrypsin-like (beta5) proteasome activities of purified human 20S proteasomes, with half-maximal inhibitory concentration (IC50) values of 7.1, 6.3, and 9.3 mumol/L, respectively. celastrol 36-45 adaptor related protein complex 5 subunit beta 1 Homo sapiens 126-131 30928629-5 2019 Celastrol also inhibited human MM cellular beta1, beta2, and beta5 proteasome activities, with IC50 values of 2.3, 2.1, and 0.9 mumol/L, respectively. celastrol 0-9 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 43-48 30928629-5 2019 Celastrol also inhibited human MM cellular beta1, beta2, and beta5 proteasome activities, with IC50 values of 2.3, 2.1, and 0.9 mumol/L, respectively. celastrol 0-9 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 50-55 30928629-5 2019 Celastrol also inhibited human MM cellular beta1, beta2, and beta5 proteasome activities, with IC50 values of 2.3, 2.1, and 0.9 mumol/L, respectively. celastrol 0-9 adaptor related protein complex 5 subunit beta 1 Homo sapiens 61-66 30821426-0 2019 The leptin sensitizer celastrol reduces age-associated obesity and modulates behavioral rhythms. celastrol 22-31 leptin Homo sapiens 4-10 30821426-4 2019 Here we demonstrate that celastrol, a natural phytochemical that was previously shown to act as a leptin sensitizer, induces weight loss in aged animals, but not in young controls. celastrol 25-34 leptin Homo sapiens 98-104 30894367-0 2019 Celastrol Reduces Obesity in MC4R Deficiency and Stimulates Sympathetic Nerve Activity Affecting Metabolic and Cardiovascular Functions. celastrol 0-9 melanocortin 4 receptor Mus musculus 29-33 30742994-0 2019 Treatment with celastrol protects against obesity through suppression of galanin-induced fat intake and activation of PGC-1alpha/GLUT4 axis-mediated glucose consumption. celastrol 15-24 galanin and GMAP prepropeptide Mus musculus 73-80 30742994-0 2019 Treatment with celastrol protects against obesity through suppression of galanin-induced fat intake and activation of PGC-1alpha/GLUT4 axis-mediated glucose consumption. celastrol 15-24 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 118-128 30742994-0 2019 Treatment with celastrol protects against obesity through suppression of galanin-induced fat intake and activation of PGC-1alpha/GLUT4 axis-mediated glucose consumption. celastrol 15-24 solute carrier family 2 (facilitated glucose transporter), member 4 Mus musculus 129-134 30742994-7 2019 More importantly, in addition to these direct anti-obesity activities, celastrol augmented the PGC-1alpha and GLUT4 expression in adipocytes and skeletal muscles to increase glucose uptake through AKT and P38 MAPK activation. celastrol 71-80 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 95-105 30742994-7 2019 More importantly, in addition to these direct anti-obesity activities, celastrol augmented the PGC-1alpha and GLUT4 expression in adipocytes and skeletal muscles to increase glucose uptake through AKT and P38 MAPK activation. celastrol 71-80 solute carrier family 2 (facilitated glucose transporter), member 4 Mus musculus 110-115 30742994-7 2019 More importantly, in addition to these direct anti-obesity activities, celastrol augmented the PGC-1alpha and GLUT4 expression in adipocytes and skeletal muscles to increase glucose uptake through AKT and P38 MAPK activation. celastrol 71-80 thymoma viral proto-oncogene 1 Mus musculus 197-200 30742994-7 2019 More importantly, in addition to these direct anti-obesity activities, celastrol augmented the PGC-1alpha and GLUT4 expression in adipocytes and skeletal muscles to increase glucose uptake through AKT and P38 MAPK activation. celastrol 71-80 mitogen-activated protein kinase 14 Mus musculus 205-213 30742994-8 2019 Celastrol also inhibited gluconeogenic activity through a CREB/PGC-1alpha pathway. celastrol 0-9 cAMP responsive element binding protein 1 Mus musculus 58-62 30742994-8 2019 Celastrol also inhibited gluconeogenic activity through a CREB/PGC-1alpha pathway. celastrol 0-9 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 63-73 30742994-9 2019 In conclusion, the weight-lowering effects of celastrol are driven by decreased galanin-induced food consumption. celastrol 46-55 galanin and GMAP prepropeptide Mus musculus 80-87 30894367-2 2019 Celastrol, a compound found in the roots of the Tripterygium wilfordii and known to reduce endoplasmic reticulum (ER) stress, has recently emerged as a promising candidate to treat obesity by improving leptin sensitivity. celastrol 0-9 leptin Mus musculus 202-208 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 leptin receptor Mus musculus 74-89 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 leptin receptor Mus musculus 91-95 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 melanocortin 4 receptor Mus musculus 107-130 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 melanocortin 4 receptor Mus musculus 132-136 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 melanocortin 4 receptor Mus musculus 263-267 30894367-4 2019 Using three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null, and melanocortin 4 receptor (MC4R)-null mice-in this study, we show that systemic celastrol administration substantially reduces food intake and body weight in MC4R-null comparable to DIO, proving the MC4R-independent antiobesity effect of celastrol. celastrol 185-194 melanocortin 4 receptor Mus musculus 263-267 30618198-0 2019 Celastrol protects human retinal pigment epithelial cells against hydrogen peroxide mediated oxidative stress, autophagy, and apoptosis through sirtuin 3 signal pathway. celastrol 0-9 sirtuin 3 Homo sapiens 144-153 30798476-0 2019 Transferrin-functionalised microemulsion co-delivery of beta-elemene and celastrol for enhanced anti-lung cancer treatment and reduced systemic toxicity. celastrol 73-82 transferrin Mus musculus 0-11 30798476-1 2019 In this study, we developed an intravenously injectable, transferrin-functionalised microemulsion that simultaneously carries beta-elemene and celastrol (called Tf-EC-MEs) for enhanced anti-lung cancer treatment and reduced systemic toxicity. celastrol 143-152 transferrin Mus musculus 57-68 30618198-8 2019 Reverse transcription polymerase chain reaction and Western blot showed that celastrol elevated the messenger RNA (mRNA) and protein expression of sirtuin 3 (SIRT3) in H2 O2 -induced ARPE-19 cells. celastrol 77-86 sirtuin 3 Homo sapiens 147-156 30618198-8 2019 Reverse transcription polymerase chain reaction and Western blot showed that celastrol elevated the messenger RNA (mRNA) and protein expression of sirtuin 3 (SIRT3) in H2 O2 -induced ARPE-19 cells. celastrol 77-86 sirtuin 3 Homo sapiens 158-163 31152143-9 2019 RESULTS Sorafenib treatment induced the compensatory activation of the AKT pathway and autocrine VEGF in hepatoma cells, which could be reversed by celastrol. celastrol 148-157 thymoma viral proto-oncogene 1 Mus musculus 71-74 30618198-9 2019 Inhibition of the level of SIRT3 by SIRT3 small interfering RNA (siRNA) reversed the effects of celastrol on oxidative stress, autophagy, and apoptosis in H2 O2 -induced ARPE-19 cells. celastrol 96-105 sirtuin 3 Homo sapiens 27-32 30618198-9 2019 Inhibition of the level of SIRT3 by SIRT3 small interfering RNA (siRNA) reversed the effects of celastrol on oxidative stress, autophagy, and apoptosis in H2 O2 -induced ARPE-19 cells. celastrol 96-105 sirtuin 3 Homo sapiens 36-41 30618198-10 2019 In conclusion, these observations suggest that celastrol activates the SIRT3 pathway in RPE cells and protects against H2 O2 -induced oxidative stress and apoptosis. celastrol 47-56 sirtuin 3 Homo sapiens 71-76 31152143-9 2019 RESULTS Sorafenib treatment induced the compensatory activation of the AKT pathway and autocrine VEGF in hepatoma cells, which could be reversed by celastrol. celastrol 148-157 vascular endothelial growth factor A Mus musculus 97-101 31152143-11 2019 CONCLUSIONS Celastrol enhances the antitumor activity of sorafenib in HCC tumor cells by suppressing the AKT pathway and VEGF autocrine system. celastrol 12-21 thymoma viral proto-oncogene 1 Mus musculus 105-108 31152143-11 2019 CONCLUSIONS Celastrol enhances the antitumor activity of sorafenib in HCC tumor cells by suppressing the AKT pathway and VEGF autocrine system. celastrol 12-21 vascular endothelial growth factor A Mus musculus 121-125 31053160-0 2019 Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 55-58 30989726-0 2019 Celastrol inhibits growth and metastasis of human gastric cancer cell MKN45 by down-regulating microRNA-21. celastrol 0-9 microRNA 21 Homo sapiens 95-106 30989726-5 2019 Under celastrol treatment, overexpression of microRNA-21 (miR-21) increased cell viability, migration, and invasion and inhibited cell apoptosis compared with negative control (p < .05, p < .01, or p < .001). celastrol 6-15 microRNA 21 Homo sapiens 45-56 30989726-5 2019 Under celastrol treatment, overexpression of microRNA-21 (miR-21) increased cell viability, migration, and invasion and inhibited cell apoptosis compared with negative control (p < .05, p < .01, or p < .001). celastrol 6-15 microRNA 21 Homo sapiens 58-64 30989726-6 2019 In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IkappaBalpha phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). celastrol 161-170 phosphatase and tensin homolog Homo sapiens 36-40 30989726-6 2019 In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IkappaBalpha phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). celastrol 161-170 AKT serine/threonine kinase 1 Homo sapiens 87-90 30989726-6 2019 In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IkappaBalpha phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). celastrol 161-170 RELA proto-oncogene, NF-kB subunit Homo sapiens 92-95 30989726-6 2019 In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IkappaBalpha phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). celastrol 161-170 NFKB inhibitor alpha Homo sapiens 101-113 30989726-6 2019 In addition, the phosphorylation of PTEN was significantly up-regulated, whereas PI3K, AKT, p65, and IkappaBalpha phosphorylation was statistically decreased by celastrol (p < .05 or p < .01) and then further reversed by miR-21 overexpression (p < .05 or p < .01). celastrol 161-170 microRNA 21 Homo sapiens 227-233 30989726-8 2019 In conclusion, celastrol inhibits proliferation, migration, and invasion and inactivates PTEN/PI3K/AKT and nuclear factor kappaB signaling pathways in MKN45 cells by down-regulating miR-21. celastrol 15-24 phosphatase and tensin homolog Homo sapiens 89-93 31053160-0 2019 Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 63-66 31053160-0 2019 Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 67-71 31053160-8 2019 Celastrol increased the formation of autophagosomes, accumulation of LC3B and the expression of p62 protein. celastrol 0-9 microtubule associated protein 1 light chain 3 beta Homo sapiens 69-73 31053160-8 2019 Celastrol increased the formation of autophagosomes, accumulation of LC3B and the expression of p62 protein. celastrol 0-9 nucleoporin 62 Homo sapiens 96-99 31053160-11 2019 Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. celastrol 13-22 mitogen-activated protein kinase 8 Homo sapiens 31-34 31053160-11 2019 Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. celastrol 13-22 AKT serine/threonine kinase 1 Homo sapiens 97-100 31053160-11 2019 Furthermore, celastrol induced JNK activation and ROS production and inhibited the activities of Akt and mTOR kinases. celastrol 13-22 mechanistic target of rapamycin kinase Homo sapiens 105-109 31053160-12 2019 JNK and ROS inhibitors significantly attenuated celastrol-trigged apoptosis and autophagy, while Akt and mTOR inhibitors had opposite effects. celastrol 48-57 mitogen-activated protein kinase 8 Homo sapiens 0-3 31053160-13 2019 CONCLUSIONS: In conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway. celastrol 52-61 mitogen-activated protein kinase 8 Homo sapiens 141-144 31053160-13 2019 CONCLUSIONS: In conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway. celastrol 52-61 AKT serine/threonine kinase 1 Homo sapiens 172-175 31053160-13 2019 CONCLUSIONS: In conclusion, our study revealed that celastrol caused G2/M phase arrest and trigged apoptosis and autophagy by activating ROS/JNK signaling and blocking the Akt/mTOR signaling pathway. celastrol 52-61 mechanistic target of rapamycin kinase Homo sapiens 176-180 30989726-8 2019 In conclusion, celastrol inhibits proliferation, migration, and invasion and inactivates PTEN/PI3K/AKT and nuclear factor kappaB signaling pathways in MKN45 cells by down-regulating miR-21. celastrol 15-24 AKT serine/threonine kinase 1 Homo sapiens 99-102 30989726-8 2019 In conclusion, celastrol inhibits proliferation, migration, and invasion and inactivates PTEN/PI3K/AKT and nuclear factor kappaB signaling pathways in MKN45 cells by down-regulating miR-21. celastrol 15-24 microRNA 21 Homo sapiens 182-188 30768745-8 2019 Our results showed that celastrol could not only reduce contents of creatinine and urea nitrogen in blood but also reduce excretion of urinary protein in diabetic rats, improve renal pathological injury, and down-regulate the expression of p38MAPK and NF-kappaB p65. celastrol 24-33 synaptotagmin 1 Rattus norvegicus 262-265 31022663-0 2019 Celastrol, a plant-derived triterpene, induces cisplatin-resistance nasopharyngeal carcinoma cancer cell apoptosis though ERK1/2 and p38 MAPK signaling pathway. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 122-128 31022663-0 2019 Celastrol, a plant-derived triterpene, induces cisplatin-resistance nasopharyngeal carcinoma cancer cell apoptosis though ERK1/2 and p38 MAPK signaling pathway. celastrol 0-9 mitogen-activated protein kinase 1 Homo sapiens 133-136 31022663-0 2019 Celastrol, a plant-derived triterpene, induces cisplatin-resistance nasopharyngeal carcinoma cancer cell apoptosis though ERK1/2 and p38 MAPK signaling pathway. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 137-141 31022663-6 2019 With further analysis, we observed that celastrol-induced activation of caspases was accompanied by increased phosphorylation of MAPK pathway proteins, p38, ERK1/2. celastrol 40-49 mitogen-activated protein kinase 3 Homo sapiens 129-133 31022663-6 2019 With further analysis, we observed that celastrol-induced activation of caspases was accompanied by increased phosphorylation of MAPK pathway proteins, p38, ERK1/2. celastrol 40-49 mitogen-activated protein kinase 1 Homo sapiens 152-155 31022663-6 2019 With further analysis, we observed that celastrol-induced activation of caspases was accompanied by increased phosphorylation of MAPK pathway proteins, p38, ERK1/2. celastrol 40-49 mitogen-activated protein kinase 3 Homo sapiens 157-163 30913029-0 2019 Tripterine inhibits proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating microRNA-15a. celastrol 0-10 microRNA 15a Homo sapiens 109-121 30913029-8 2019 Moreover, tripterine up-regulated the expression of miR-15a in a concentration-dependent manner and miR-15a participated in the effects of tripterine on MDA-MB-231 cell proliferation, migration, invasion and apoptosis. celastrol 10-20 microRNA 15a Homo sapiens 52-59 30913029-8 2019 Moreover, tripterine up-regulated the expression of miR-15a in a concentration-dependent manner and miR-15a participated in the effects of tripterine on MDA-MB-231 cell proliferation, migration, invasion and apoptosis. celastrol 139-149 microRNA 15a Homo sapiens 100-107 30913029-9 2019 In addition, tripterine inactivated PI3K/AKT and JNK pathways in MDA-MB-231 cells by up-regulating miR-15a. celastrol 13-23 AKT serine/threonine kinase 1 Homo sapiens 41-44 30913029-9 2019 In addition, tripterine inactivated PI3K/AKT and JNK pathways in MDA-MB-231 cells by up-regulating miR-15a. celastrol 13-23 mitogen-activated protein kinase 8 Homo sapiens 49-52 30913029-9 2019 In addition, tripterine inactivated PI3K/AKT and JNK pathways in MDA-MB-231 cells by up-regulating miR-15a. celastrol 13-23 microRNA 15a Homo sapiens 99-106 30913029-10 2019 In conclusion, tripterine inhibited proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating miR-15a and inactivating PI3K/AKT and JNK pathways. celastrol 15-25 microRNA 15a Homo sapiens 125-132 30913029-10 2019 In conclusion, tripterine inhibited proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating miR-15a and inactivating PI3K/AKT and JNK pathways. celastrol 15-25 AKT serine/threonine kinase 1 Homo sapiens 155-158 30913029-10 2019 In conclusion, tripterine inhibited proliferation, migration and invasion of breast cancer MDA-MB-231 cells by up-regulating miR-15a and inactivating PI3K/AKT and JNK pathways. celastrol 15-25 mitogen-activated protein kinase 8 Homo sapiens 163-166 30820608-0 2019 Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 67-71 30820608-0 2019 Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology. celastrol 0-9 serum/glucocorticoid regulated kinase 1 Mus musculus 72-76 30820608-3 2019 We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice. celastrol 80-89 mitogen-activated protein kinase 1 Mus musculus 126-130 30820608-3 2019 We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice. celastrol 80-89 serum/glucocorticoid regulated kinase 1 Mus musculus 179-218 30820608-3 2019 We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice. celastrol 80-89 serum/glucocorticoid regulated kinase 1 Mus musculus 220-224 30820608-3 2019 We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice. celastrol 80-89 brain derived neurotrophic factor Mus musculus 286-319 30820608-3 2019 We describe here a gene expression- and bioinformatics-based study showing that celastrol, a natural triterpenoid, acting via MAPK pathway regulates the downstream genes encoding serum/glucocorticoid regulated kinase 1 (SGK1), which plays a vital role in Th17/Treg differentiation, and brain-derived neurotrophic factor (BDNF), which is a neurotrophic factor, thereby offering protection against experimental autoimmune encephalomyelitis (EAE) in mice. celastrol 80-89 brain derived neurotrophic factor Mus musculus 321-325 30820608-5 2019 RESULTS: Interestingly, celastrol reversed the expression of many MOG-induced genes involved in inflammation and immune pathology. celastrol 24-33 myelin oligodendrocyte glycoprotein Mus musculus 66-69 30820608-6 2019 The MAPK pathway involving p38MAPK and ERK was identified as one of the mediators of celastrol action. celastrol 85-94 mitogen-activated protein kinase 1 Mus musculus 4-8 30820608-6 2019 The MAPK pathway involving p38MAPK and ERK was identified as one of the mediators of celastrol action. celastrol 85-94 mitogen-activated protein kinase 14 Mus musculus 27-34 30820608-6 2019 The MAPK pathway involving p38MAPK and ERK was identified as one of the mediators of celastrol action. celastrol 85-94 mitogen-activated protein kinase 1 Mus musculus 39-42 30833749-0 2019 IL1R1 is required for celastrol"s leptin-sensitization and antiobesity effects. celastrol 22-31 interleukin 1 receptor, type I Mus musculus 0-5 30833749-1 2019 Celastrol, a pentacyclic triterpene, is the most potent antiobesity agent that has been reported thus far1. celastrol 0-9 fatty acyl CoA reductase 1 Mus musculus 102-106 30833749-3 2019 In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol"s action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. celastrol 79-88 interleukin 1 receptor, type I Mus musculus 29-53 30833749-3 2019 In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol"s action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. celastrol 79-88 interleukin 1 receptor, type I Mus musculus 55-60 30833749-3 2019 In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol"s action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. celastrol 173-182 interleukin 1 receptor, type I Mus musculus 29-53 30833749-3 2019 In this study, we identified interleukin-1 receptor 1 (IL1R1) as a mediator of celastrol"s action by using temporally resolved analysis of the hypothalamic transcriptome in celastrol-treated DIO, lean, and db/db mice. celastrol 173-182 interleukin 1 receptor, type I Mus musculus 55-60 30833749-4 2019 We demonstrate that IL1R1-deficient mice are completely resistant to the effects of celastrol in leptin sensitization and treatment of obesity, diabetes, and nonalcoholic steatohepatitis. celastrol 84-93 interleukin 1 receptor, type I Mus musculus 20-25 30833749-5 2019 Thus, we conclude that IL1R1 is a gatekeeper for celastrol"s metabolic actions. celastrol 49-58 interleukin 1 receptor, type I Mus musculus 23-28 30798158-0 2019 Celastrol ameliorates Aspergillus fumigatus keratitis via inhibiting LOX-1. celastrol 0-9 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 69-74 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 interleukin 1 beta Mus musculus 91-99 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 tumor necrosis factor Mus musculus 101-110 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 interleukin 10 Mus musculus 112-117 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 transforming growth factor, beta 1 Mus musculus 119-127 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 chemokine (C-X-C motif) ligand 2 Mus musculus 129-134 30798158-7 2019 RESULTS: C57BL/6 mice treated with CLT from 1 day post infection showed decreased disease, IL-1beta, TNF-alpha, IL-10, TGF-beta, MIP-2 and LOX-1 levels. celastrol 35-38 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 139-144 30798158-10 2019 CONCLUSION: These data provide evidences that CLT ameliorates A. fumigatus keratitis of C57BL/6 mice via inhibiting LOX-1. celastrol 46-49 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 116-121 30287053-0 2019 Celastrol Reverses Palmitic Acid-Induced Insulin Resistance in HepG2 Cells via Restoring the miR-223 and GLUT4 Pathway. celastrol 0-9 insulin Homo sapiens 41-48 30287053-0 2019 Celastrol Reverses Palmitic Acid-Induced Insulin Resistance in HepG2 Cells via Restoring the miR-223 and GLUT4 Pathway. celastrol 0-9 microRNA 223 Homo sapiens 93-100 30287053-0 2019 Celastrol Reverses Palmitic Acid-Induced Insulin Resistance in HepG2 Cells via Restoring the miR-223 and GLUT4 Pathway. celastrol 0-9 solute carrier family 2 member 4 Homo sapiens 105-110 30287053-1 2019 OBJECTIVES: The natural triterpenoid compound celastrol ameliorates insulin resistance (IR) in animal models, but the underlying molecular mechanism is unclear. celastrol 46-55 insulin Homo sapiens 68-75 30287053-6 2019 The PA-induced GLUT4 and IRS1 downregulation and Ser307 phosphorylation on IRS1 was reversed by subsequent treatment with 600 nM celastrol for 6 h. We next investigated which IR-related miRNAs were possible upstream regulators of celastrol-mediated reversal of PA-induced HepG2 IR. celastrol 129-138 solute carrier family 2 member 4 Homo sapiens 15-20 30287053-6 2019 The PA-induced GLUT4 and IRS1 downregulation and Ser307 phosphorylation on IRS1 was reversed by subsequent treatment with 600 nM celastrol for 6 h. We next investigated which IR-related miRNAs were possible upstream regulators of celastrol-mediated reversal of PA-induced HepG2 IR. celastrol 129-138 insulin receptor substrate 1 Homo sapiens 75-79 30287053-7 2019 Two miRNAs, miR-150 and -223, were significantly downregulated by PA and were re-raised by subsequent celastrol treatment; and miR-223 was upstream of miR-150. celastrol 102-111 microRNA 150 Homo sapiens 12-28 30287053-7 2019 Two miRNAs, miR-150 and -223, were significantly downregulated by PA and were re-raised by subsequent celastrol treatment; and miR-223 was upstream of miR-150. celastrol 102-111 microRNA 150 Homo sapiens 12-19 30287053-8 2019 Moreover, knocking down miR-223 abolished celastrol"s anti-IR effects in the PA-induced model. celastrol 42-51 microRNA 223 Homo sapiens 24-31 30287053-9 2019 CONCLUSIONS: Collectively, our results demonstrated that celastrol reverses PA-induced IR-related alterations, in part via miR-223 in HepG2 cells. celastrol 57-66 microRNA 223 Homo sapiens 123-130 30816529-0 2019 Axl is a novel target of celastrol that inhibits cell proliferation and migration, and increases the cytotoxicity of gefitinib in EGFR mutant non-small cell lung cancer cells. celastrol 25-34 AXL receptor tyrosine kinase Homo sapiens 0-3 30816529-5 2019 The inhibitory effect of celastrol on Axl protein expression level, cell viability and clonogenicity were identified in parental and gefitinib-resistant PC-9 cells. celastrol 25-34 AXL receptor tyrosine kinase Homo sapiens 38-41 30816529-5 2019 The inhibitory effect of celastrol on Axl protein expression level, cell viability and clonogenicity were identified in parental and gefitinib-resistant PC-9 cells. celastrol 25-34 proprotein convertase subtilisin/kexin type 9 Homo sapiens 153-157 30816529-6 2019 In addition, treatment of PC-9/GR cells with celastrol and gefitinib in combination was demonstrated to synergistically suppress Axl protein expression level, cell proliferation and migration. celastrol 45-54 proprotein convertase subtilisin/kexin type 9 Homo sapiens 26-30 30816529-6 2019 In addition, treatment of PC-9/GR cells with celastrol and gefitinib in combination was demonstrated to synergistically suppress Axl protein expression level, cell proliferation and migration. celastrol 45-54 AXL receptor tyrosine kinase Homo sapiens 129-132 30816529-8 2019 Furthermore, celastrol targets Axl to exert its anticancer effects in order to increase the susceptibility of PC-9/GR cells to gefitinib and overcome chemoresistance. celastrol 13-22 AXL receptor tyrosine kinase Homo sapiens 31-34 30816529-8 2019 Furthermore, celastrol targets Axl to exert its anticancer effects in order to increase the susceptibility of PC-9/GR cells to gefitinib and overcome chemoresistance. celastrol 13-22 proprotein convertase subtilisin/kexin type 9 Homo sapiens 110-114 30396268-9 2019 Celastrol treatment had no impact on kindling progression but reduced postkindling seizure thresholds and enhanced microglia activation in CA1 and CA3. celastrol 0-9 carbonic anhydrase 1 Mus musculus 139-142 30396268-9 2019 Celastrol treatment had no impact on kindling progression but reduced postkindling seizure thresholds and enhanced microglia activation in CA1 and CA3. celastrol 0-9 carbonic anhydrase 3 Mus musculus 147-150 30773944-6 2019 In this study, we investigated the effects and mechanism of celastrol on nitric oxide synthase (NOS) and the angiogenesis pathway in colorectal cancer. celastrol 60-69 nitric oxide synthase 2 Homo sapiens 73-94 30635274-1 2019 Celastrol-Induced Weight Loss Is Driven by Hypophagia and Independent From UCP1. celastrol 0-9 uncoupling protein 1 Homo sapiens 75-79 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 thymidine phosphorylase Homo sapiens 148-152 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 cadherin 5 Homo sapiens 154-158 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 thrombospondin 2 Homo sapiens 160-165 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 leptin Homo sapiens 167-170 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 matrix metallopeptidase 9 Homo sapiens 172-176 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 tumor necrosis factor Homo sapiens 182-185 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 interleukin 1 beta Homo sapiens 201-206 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 matrix metallopeptidase 9 Homo sapiens 208-213 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 serpin family E member 1 Homo sapiens 221-230 30773944-9 2019 Treatment with celastrol inhibited colorectal cancer cell growth and migration, and was associated with suppression of the expression of key genes (TYMP, CDH5, THBS2, LEP, MMP9, and TNF) and proteins (IL-1b, MMP-9, PDGF, Serpin E1, and TIMP-4) involved in the angiogenesis pathway. celastrol 15-24 TIMP metallopeptidase inhibitor 4 Homo sapiens 236-242 30596540-7 2019 RESULTS: Celastrol significantly inhibited LPS-induced expression of protein and mRNA expression levels encoding the proinflammatory cytokines, IL-6, IL-8, and MCP-1, in both HRPE and ARPE-19 cells. celastrol 9-18 interleukin 6 Mus musculus 144-148 30596540-7 2019 RESULTS: Celastrol significantly inhibited LPS-induced expression of protein and mRNA expression levels encoding the proinflammatory cytokines, IL-6, IL-8, and MCP-1, in both HRPE and ARPE-19 cells. celastrol 9-18 chemokine (C-X-C motif) ligand 15 Mus musculus 150-154 30596540-7 2019 RESULTS: Celastrol significantly inhibited LPS-induced expression of protein and mRNA expression levels encoding the proinflammatory cytokines, IL-6, IL-8, and MCP-1, in both HRPE and ARPE-19 cells. celastrol 9-18 mast cell protease 1 Mus musculus 160-165 30596540-8 2019 Cell viability and apoptosis assays revealed that celastrol had no apparent cytotoxic effect and it inhibited apoptosis of RPE cells at concentrations of less than 1 muM. celastrol 50-59 latexin Homo sapiens 166-169 30596540-9 2019 Mechanistically, RPE cells that were pretreated with celastrol exhibited a substantial decrease in phosphorylation of the NF-kappaB pathway regulators, IKKalpha/beta and IkappaBalpha, and subsequently inactivated P65, suggesting that celastrol ameliorates LPS-induced inflammation by suppressing the NF-kappaB signaling pathway. celastrol 53-62 RELA proto-oncogene, NF-kB subunit Homo sapiens 213-216 30706713-9 2019 The mRNAs encoded by hepatic genes associated with lipid synthesis and catabolism, including Lpcat1, Pld1, Smpd3, and Sptc2, were altered in tyloxapol-induced hyperlipidemia, and significantly recovered by celastrol treatment. celastrol 206-215 lysophosphatidylcholine acyltransferase 1 Mus musculus 93-99 30617157-7 2019 These observations demonstrated a novel role for celastrol in protecting against cholestatic liver injury through modulation of the SIRT1 and FXR. celastrol 49-58 sirtuin 1 Mus musculus 132-137 30706713-9 2019 The mRNAs encoded by hepatic genes associated with lipid synthesis and catabolism, including Lpcat1, Pld1, Smpd3, and Sptc2, were altered in tyloxapol-induced hyperlipidemia, and significantly recovered by celastrol treatment. celastrol 206-215 phospholipase D1 Mus musculus 101-105 30706713-9 2019 The mRNAs encoded by hepatic genes associated with lipid synthesis and catabolism, including Lpcat1, Pld1, Smpd3, and Sptc2, were altered in tyloxapol-induced hyperlipidemia, and significantly recovered by celastrol treatment. celastrol 206-215 sphingomyelin phosphodiesterase 3, neutral Mus musculus 107-112 30706713-10 2019 The effect of celastrol on lipid metabolism was significantly reduced in Fxr-null mice, resulting in decreased Cers6 and Acer2 mRNAs compared to wild-type mice. celastrol 14-23 nuclear receptor subfamily 1, group H, member 4 Mus musculus 73-76 30706713-10 2019 The effect of celastrol on lipid metabolism was significantly reduced in Fxr-null mice, resulting in decreased Cers6 and Acer2 mRNAs compared to wild-type mice. celastrol 14-23 ceramide synthase 6 Mus musculus 111-116 30706713-10 2019 The effect of celastrol on lipid metabolism was significantly reduced in Fxr-null mice, resulting in decreased Cers6 and Acer2 mRNAs compared to wild-type mice. celastrol 14-23 alkaline ceramidase 2 Mus musculus 121-126 30706713-11 2019 These results establish that FXR was responsible in part for the effects of celastrol in controlling lipid metabolism and contributing to the recovery of aberrant lipid metabolism in obesity-related metabolic disorders. celastrol 76-85 nuclear receptor subfamily 1, group H, member 4 Mus musculus 29-32 30617157-7 2019 These observations demonstrated a novel role for celastrol in protecting against cholestatic liver injury through modulation of the SIRT1 and FXR. celastrol 49-58 nuclear receptor subfamily 1, group H, member 4 Mus musculus 142-145 30617157-0 2019 Celastrol Protects From Cholestatic Liver Injury Through Modulation of SIRT1-FXR Signaling. celastrol 0-9 sirtuin 1 Mus musculus 71-76 30617157-0 2019 Celastrol Protects From Cholestatic Liver Injury Through Modulation of SIRT1-FXR Signaling. celastrol 0-9 nuclear receptor subfamily 1, group H, member 4 Mus musculus 77-80 30617157-4 2019 Celastrol was found to activate sirtuin 1 (SIRT1), increase farnesoid X receptor (FXR) signaling and inhibit nuclear factor-kappa B and P53 signaling. celastrol 0-9 sirtuin 1 Mus musculus 32-41 30617157-4 2019 Celastrol was found to activate sirtuin 1 (SIRT1), increase farnesoid X receptor (FXR) signaling and inhibit nuclear factor-kappa B and P53 signaling. celastrol 0-9 sirtuin 1 Mus musculus 43-48 30617157-4 2019 Celastrol was found to activate sirtuin 1 (SIRT1), increase farnesoid X receptor (FXR) signaling and inhibit nuclear factor-kappa B and P53 signaling. celastrol 0-9 nuclear receptor subfamily 1, group H, member 4 Mus musculus 82-85 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 cytochrome c, somatic Homo sapiens 110-122 30617157-4 2019 Celastrol was found to activate sirtuin 1 (SIRT1), increase farnesoid X receptor (FXR) signaling and inhibit nuclear factor-kappa B and P53 signaling. celastrol 0-9 transformation related protein 53, pseudogene Mus musculus 136-139 30617157-5 2019 The protective role of celastrol in cholestatic liver injury was diminished in mice on co-administration of SIRT1 inhibitors. celastrol 23-32 sirtuin 1 Mus musculus 108-113 30617157-6 2019 Further, the effects of celastrol on cholestatic liver injury were dramatically decreased in Fxr-null mice, suggesting that the SIRT1-FXR signaling pathway mediates the protective effects of celastrol. celastrol 24-33 nuclear receptor subfamily 1, group H, member 4 Mus musculus 93-96 30617157-6 2019 Further, the effects of celastrol on cholestatic liver injury were dramatically decreased in Fxr-null mice, suggesting that the SIRT1-FXR signaling pathway mediates the protective effects of celastrol. celastrol 191-200 nuclear receptor subfamily 1, group H, member 4 Mus musculus 93-96 30617157-6 2019 Further, the effects of celastrol on cholestatic liver injury were dramatically decreased in Fxr-null mice, suggesting that the SIRT1-FXR signaling pathway mediates the protective effects of celastrol. celastrol 191-200 sirtuin 1 Mus musculus 128-133 30617157-6 2019 Further, the effects of celastrol on cholestatic liver injury were dramatically decreased in Fxr-null mice, suggesting that the SIRT1-FXR signaling pathway mediates the protective effects of celastrol. celastrol 191-200 nuclear receptor subfamily 1, group H, member 4 Mus musculus 134-137 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 caspase 3 Homo sapiens 124-133 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 CCAAT enhancer binding protein alpha Homo sapiens 138-143 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 BCL2 apoptosis regulator Homo sapiens 200-205 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 caspase 9 Homo sapiens 273-282 30867764-9 2019 In addition, it was observed that celastrol/cisplatin upregulated the expression of Bcl-associated X protein, cytochrome c, caspase-3 and C/EBP homologous protein, and downregulated the expression of Bcl-2, poly(ADP-ribose) polymerase, 78 kDa glucose-regulated protein and caspase-9, whereas the expression of caspase-8 remained unchanged. celastrol 34-43 caspase 8 Homo sapiens 310-319 30666129-0 2019 Celastrol inhibits colorectal cancer through TGF-beta1/Smad signaling. celastrol 0-9 transforming growth factor beta 1 Homo sapiens 45-54 30668359-0 2019 Celastrol induces vincristine multidrug resistance oral cancer cell apoptosis by targeting JNK1/2 signaling pathway. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 91-95 30668359-10 2019 The present study demonstrated that celastrol triggered apoptotic cell death by inducing cell cycle arrest at the G2/M phase via the intrinsic and extrinsic pathways (increased cleaved caspase-3, caspase-8, caspase-9, and PARP). celastrol 36-45 caspase 3 Homo sapiens 185-194 30668359-10 2019 The present study demonstrated that celastrol triggered apoptotic cell death by inducing cell cycle arrest at the G2/M phase via the intrinsic and extrinsic pathways (increased cleaved caspase-3, caspase-8, caspase-9, and PARP). celastrol 36-45 caspase 8 Homo sapiens 196-205 30668359-10 2019 The present study demonstrated that celastrol triggered apoptotic cell death by inducing cell cycle arrest at the G2/M phase via the intrinsic and extrinsic pathways (increased cleaved caspase-3, caspase-8, caspase-9, and PARP). celastrol 36-45 caspase 9 Homo sapiens 207-216 30668359-10 2019 The present study demonstrated that celastrol triggered apoptotic cell death by inducing cell cycle arrest at the G2/M phase via the intrinsic and extrinsic pathways (increased cleaved caspase-3, caspase-8, caspase-9, and PARP). celastrol 36-45 collagen type XI alpha 2 chain Homo sapiens 222-226 30668359-12 2019 Celastrol mediated cell apoptosis through the downregulation of the expression of Bcl-2, not Bcl-xL. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 82-87 30668359-13 2019 Moreover, JNK1/2 signaling was the main pathway of celastrol-induced apoptosis. celastrol 51-60 mitogen-activated protein kinase 8 Homo sapiens 10-14 31933862-13 2019 Furthermore, after CEL treatment, TUNEL-positive cells, the protein level of Bax and caspase-3 activity reduced, and the level of Bcl-xl in protein increased. celastrol 19-22 BCL2 associated X, apoptosis regulator Rattus norvegicus 77-80 31933862-13 2019 Furthermore, after CEL treatment, TUNEL-positive cells, the protein level of Bax and caspase-3 activity reduced, and the level of Bcl-xl in protein increased. celastrol 19-22 caspase 3 Rattus norvegicus 85-94 31933862-13 2019 Furthermore, after CEL treatment, TUNEL-positive cells, the protein level of Bax and caspase-3 activity reduced, and the level of Bcl-xl in protein increased. celastrol 19-22 Bcl2-like 1 Rattus norvegicus 130-136 30709873-0 2019 Correction: Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway. celastrol 12-21 AKT serine/threonine kinase 1 Homo sapiens 90-93 30709873-0 2019 Correction: Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway. celastrol 12-21 mechanistic target of rapamycin kinase Homo sapiens 94-123 30569150-0 2019 Autophagy flux inhibition mediated by celastrol sensitized lung cancer cells to TRAIL-induced apoptosis via regulation of mitochondrial transmembrane potential and reactive oxygen species. celastrol 38-47 TNF superfamily member 10 Homo sapiens 80-85 30569150-3 2019 The present study demonstrated that the anti-cancer and anti-inflammatory drug celastrol, through its anti-metastatic properties, may initiate TRAIL-mediated apoptotic cell death in lung cancer cells. celastrol 79-88 TNF superfamily member 10 Homo sapiens 143-148 30569150-5 2019 Notably, treatment with celastrol caused an increase in microtubule-associated proteins 1A/1B light chain 3B-II and p62 levels, whereas co-treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. celastrol 24-33 nucleoporin 62 Homo sapiens 116-119 30569150-5 2019 Notably, treatment with celastrol caused an increase in microtubule-associated proteins 1A/1B light chain 3B-II and p62 levels, whereas co-treatment of celastrol and TRAIL increased active caspase 3 and 8 levels compared with the control, confirming inhibited autophagy flux. celastrol 152-161 caspase 3 Homo sapiens 189-198 30569150-6 2019 The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL-resistant lung cancer, suggesting that celastrol-mediated autophagy flux inhibition sensitized TRAIL-initiated apoptosis via regulation of ROS and DeltaPsim. celastrol 31-40 TNF superfamily member 10 Homo sapiens 117-122 30569150-6 2019 The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL-resistant lung cancer, suggesting that celastrol-mediated autophagy flux inhibition sensitized TRAIL-initiated apoptosis via regulation of ROS and DeltaPsim. celastrol 31-40 TNF superfamily member 10 Homo sapiens 117-122 30569150-6 2019 The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL-resistant lung cancer, suggesting that celastrol-mediated autophagy flux inhibition sensitized TRAIL-initiated apoptosis via regulation of ROS and DeltaPsim. celastrol 162-171 TNF superfamily member 10 Homo sapiens 20-25 30569150-6 2019 The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL-resistant lung cancer, suggesting that celastrol-mediated autophagy flux inhibition sensitized TRAIL-initiated apoptosis via regulation of ROS and DeltaPsim. celastrol 162-171 TNF superfamily member 10 Homo sapiens 117-122 30569150-6 2019 The combined use of TRAIL with celastrol may serve as a safe and adequate therapeutic technique for the treatment of TRAIL-resistant lung cancer, suggesting that celastrol-mediated autophagy flux inhibition sensitized TRAIL-initiated apoptosis via regulation of ROS and DeltaPsim. celastrol 162-171 TNF superfamily member 10 Homo sapiens 117-122 30601470-1 2019 In this work, the hydrophobic small molecule NF-kappaB inhibitor celastrol was loaded into poly(ethylene glycol)-b-poly(propylene sulfide) (PEG-b-PPS) micelles. celastrol 65-74 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 45-54 30601470-3 2019 Encapsulation of celastrol within these nanocarriers significantly reduced cytotoxicity compared to free celastrol, while simultaneously expanding the lower concentration range for effective inhibition of NF-kappaB signaling by nearly 50 000-fold. celastrol 17-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 205-214 30601470-4 2019 Furthermore, celastrol-loaded micelles successfully reduced TNF-alpha secretion after LPS stimulation of RAW 264.7 cells and reduced the number of neutrophils and inflammatory monocytes within atherosclerotic plaques of ldlr-/- mice. celastrol 13-22 tumor necrosis factor Mus musculus 60-69 30601470-4 2019 Furthermore, celastrol-loaded micelles successfully reduced TNF-alpha secretion after LPS stimulation of RAW 264.7 cells and reduced the number of neutrophils and inflammatory monocytes within atherosclerotic plaques of ldlr-/- mice. celastrol 13-22 low density lipoprotein receptor Mus musculus 220-224 30666129-0 2019 Celastrol inhibits colorectal cancer through TGF-beta1/Smad signaling. celastrol 0-9 SMAD family member 4 Homo sapiens 55-59 30666129-3 2019 Importantly, celastrol, a major components of the root extract of the traditional Chinese herb Tripterygium wilfordii Hook F, has been shown to inhibit the growth, adhesion, and metastasis of human CRC cells through the inhibition of TGF-beta1/Smad signaling. celastrol 13-22 transforming growth factor beta 1 Homo sapiens 234-243 30666129-3 2019 Importantly, celastrol, a major components of the root extract of the traditional Chinese herb Tripterygium wilfordii Hook F, has been shown to inhibit the growth, adhesion, and metastasis of human CRC cells through the inhibition of TGF-beta1/Smad signaling. celastrol 13-22 SMAD family member 4 Homo sapiens 244-248 30666129-5 2019 Results: Our results indicated that celastrol can reduce the expression levels of TGF-beta1, TGFbetaRI, and TGFbetaRII in HCT116 and SW620 cells. celastrol 36-45 transforming growth factor beta 1 Homo sapiens 82-91 30666129-5 2019 Results: Our results indicated that celastrol can reduce the expression levels of TGF-beta1, TGFbetaRI, and TGFbetaRII in HCT116 and SW620 cells. celastrol 36-45 transforming growth factor beta receptor 1 Homo sapiens 93-102 30666129-5 2019 Results: Our results indicated that celastrol can reduce the expression levels of TGF-beta1, TGFbetaRI, and TGFbetaRII in HCT116 and SW620 cells. celastrol 36-45 transforming growth factor beta receptor 2 Homo sapiens 108-118 30666129-6 2019 Furthermore, celastrol could also prevent the increase in Smad4 and p-Smad2/3 in HCT116 and SW620 cells. celastrol 13-22 SMAD family member 4 Homo sapiens 58-63 30666129-6 2019 Furthermore, celastrol could also prevent the increase in Smad4 and p-Smad2/3 in HCT116 and SW620 cells. celastrol 13-22 SMAD family member 3 Homo sapiens 70-77 30666129-7 2019 Conclusion: Celastrol could inhibit tumor growth through TGF-beta1/Smad signaling and might be a promising therapeutic component against CRC. celastrol 12-21 transforming growth factor beta 1 Homo sapiens 57-66 30666129-7 2019 Conclusion: Celastrol could inhibit tumor growth through TGF-beta1/Smad signaling and might be a promising therapeutic component against CRC. celastrol 12-21 SMAD family member 4 Homo sapiens 67-71 30472522-5 2019 Celastrol simultaneously reduced the activation of microglia (especially M1 microglia) in the spinal cord, inhibited the pyroptosis-related proteins (NLRP3 ASC Caspase-1 GSDMD), reduced the release of TNF-alpha IL-1beta and IL-18 inflammatory factors, and increased the release of IL10 cytokines. celastrol 0-9 NLR family, pyrin domain containing 3 Rattus norvegicus 150-155 30395883-0 2019 Celastrol ameliorates inflammatory pain and modulates HMGB1/NF-kappaB signaling pathway in dorsal root ganglion. celastrol 0-9 high mobility group box 1 Rattus norvegicus 54-59 30395883-3 2019 We aim to investigate whether HMGB1 in dorsal root ganglion (DRG) participates in the effect of celastrol on inflammatory pain. celastrol 96-105 high mobility group box 1 Rattus norvegicus 30-35 30395883-8 2019 These results showed that celastrol significantly suppressed HMGB1, NF-kappaB and IL-1beta mRNA and protein expression in DRG and alleviated CFA-evoked thermal hyperalgesia. celastrol 26-35 high mobility group box 1 Rattus norvegicus 61-66 30395883-8 2019 These results showed that celastrol significantly suppressed HMGB1, NF-kappaB and IL-1beta mRNA and protein expression in DRG and alleviated CFA-evoked thermal hyperalgesia. celastrol 26-35 interleukin 1 beta Rattus norvegicus 82-90 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 cytochrome c oxidase II, mitochondrial Rattus norvegicus 43-48 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 interleukin 6 Rattus norvegicus 87-91 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 interleukin 17A Rattus norvegicus 93-98 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 tumor necrosis factor Rattus norvegicus 100-109 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 mast cell protease 1-like 1 Rattus norvegicus 111-116 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 glial fibrillary acidic protein Rattus norvegicus 118-122 30395883-9 2019 Furthermore, celastrol obviously inhibited COX-2 protein expression and down-regulated IL-6, IL-17, TNF-alpha, MCP-1, GFAP and CD11b mRNA levels in DRG of CFA rats. celastrol 13-22 integrin subunit alpha M Rattus norvegicus 127-132 30395883-10 2019 Collectively, the present study firstly provide evidences of the anti-inflammatory effect of celastrol via suppressing CFA-induced the activation of HMGB1/NF-kappaB signaling pathway in DRG, which maybe a potential therapeutic target for celastrol alleviating inflammatory pain. celastrol 93-102 high mobility group box 1 Rattus norvegicus 149-154 30362615-0 2019 Pharmacological induction of Heat Shock Protein 70 by celastrol protects motoneurons from excitotoxicity in rat spinal cord in vitro. celastrol 54-63 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 29-50 30362615-5 2019 Despite its narrow range of drug safety in vitro, celastrol was not toxic to the rat spinal cord at 0.75 muM concentration and enhanced the expression of HSP70 by motoneurons. celastrol 50-59 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 154-159 30791741-0 2019 Tripterine up-regulates miR-223 to alleviate lipopolysaccharide-induced damage in murine chondrogenic ATDC5 cells. celastrol 0-10 microRNA 223 Mus musculus 24-31 30791741-8 2019 Tripterine protected ATDC5 cells against LPS-induced chondrocyte loss and the release of IL-6 and TNF-alpha. celastrol 0-10 interleukin 6 Mus musculus 89-93 30791741-8 2019 Tripterine protected ATDC5 cells against LPS-induced chondrocyte loss and the release of IL-6 and TNF-alpha. celastrol 0-10 tumor necrosis factor Mus musculus 98-107 30791741-9 2019 miR-223 was down-regulated by LPS, while was up-regulated by tripterine. celastrol 61-71 microRNA 223 Mus musculus 0-7 30791741-10 2019 The protective actions of tripterine were eliminated when miR-223 was silenced. celastrol 26-36 microRNA 223 Mus musculus 58-65 30791741-11 2019 Besides, tripterine inhibited hypertrophic differentiation induced by LPS, and the inhibitory effects of tripterine on hypertrophic differentiation could be abolished when miR-223 was silenced. celastrol 105-115 microRNA 223 Mus musculus 172-179 30791741-12 2019 Furthermore, tripterine activated PI3K/AKT pathway and deactivated NF-kappaB pathway. celastrol 13-23 thymoma viral proto-oncogene 1 Mus musculus 39-42 30791741-12 2019 Furthermore, tripterine activated PI3K/AKT pathway and deactivated NF-kappaB pathway. celastrol 13-23 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 67-76 30791741-13 2019 And the regulatory effects of tripterine on these two pathways were abolished by miR-223 silence. celastrol 30-40 microRNA 223 Mus musculus 81-88 30791741-14 2019 This study revealed that tripterine protected ATDC5 cells against LPS-induced cell damage possibly via up-regulation of miR-223 and modulation of NF-kappaB and PI3K/AKT pathways. celastrol 25-35 microRNA 223 Mus musculus 120-127 30791741-14 2019 This study revealed that tripterine protected ATDC5 cells against LPS-induced cell damage possibly via up-regulation of miR-223 and modulation of NF-kappaB and PI3K/AKT pathways. celastrol 25-35 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 146-155 30791741-14 2019 This study revealed that tripterine protected ATDC5 cells against LPS-induced cell damage possibly via up-regulation of miR-223 and modulation of NF-kappaB and PI3K/AKT pathways. celastrol 25-35 thymoma viral proto-oncogene 1 Mus musculus 165-168 30353639-6 2019 In addition, EA potentiated the inhibitory effects of the natural compound celastrol on lung cancer cells in vitro and in vivo by enhancing autophagy and down-regulating CIP2A. celastrol 75-84 cell proliferation regulating inhibitor of protein phosphatase 2A Mus musculus 170-175 30389635-0 2019 Celastrol strongly inhibits proliferation, migration and cancer stem cell properties through suppression of Pin1 in ovarian cancer cells. celastrol 0-9 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 108-112 30389635-5 2019 Celastrol resulted in a G2/M cell cycle arrest, accompanied with the down-regulation of Cyclin D1, CDK2, and CDK4. celastrol 0-9 cyclin D1 Homo sapiens 88-97 30389635-5 2019 Celastrol resulted in a G2/M cell cycle arrest, accompanied with the down-regulation of Cyclin D1, CDK2, and CDK4. celastrol 0-9 cyclin dependent kinase 2 Homo sapiens 99-103 30389635-5 2019 Celastrol resulted in a G2/M cell cycle arrest, accompanied with the down-regulation of Cyclin D1, CDK2, and CDK4. celastrol 0-9 cyclin dependent kinase 4 Homo sapiens 109-113 30389635-6 2019 Celastrol induced apoptosis primarily via up-regulation of caspase-3, caspase-8, and Bax, and down-regulation of Bcl-2. celastrol 0-9 caspase 3 Homo sapiens 59-68 30389635-6 2019 Celastrol induced apoptosis primarily via up-regulation of caspase-3, caspase-8, and Bax, and down-regulation of Bcl-2. celastrol 0-9 caspase 8 Homo sapiens 70-79 30389635-6 2019 Celastrol induced apoptosis primarily via up-regulation of caspase-3, caspase-8, and Bax, and down-regulation of Bcl-2. celastrol 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 85-88 30389635-6 2019 Celastrol induced apoptosis primarily via up-regulation of caspase-3, caspase-8, and Bax, and down-regulation of Bcl-2. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 113-118 30389635-7 2019 Celastrol treatment inhibited the expression of stem cell marker CD44, Nanog, Klf4, and Oct4, and reduced a portion of the CD44highCD24low cell population. celastrol 0-9 CD44 molecule (Indian blood group) Homo sapiens 65-69 30389635-7 2019 Celastrol treatment inhibited the expression of stem cell marker CD44, Nanog, Klf4, and Oct4, and reduced a portion of the CD44highCD24low cell population. celastrol 0-9 Nanog homeobox Homo sapiens 71-76 30389635-7 2019 Celastrol treatment inhibited the expression of stem cell marker CD44, Nanog, Klf4, and Oct4, and reduced a portion of the CD44highCD24low cell population. celastrol 0-9 Kruppel like factor 4 Homo sapiens 78-82 30389635-7 2019 Celastrol treatment inhibited the expression of stem cell marker CD44, Nanog, Klf4, and Oct4, and reduced a portion of the CD44highCD24low cell population. celastrol 0-9 POU class 5 homeobox 1 Homo sapiens 88-92 30389635-7 2019 Celastrol treatment inhibited the expression of stem cell marker CD44, Nanog, Klf4, and Oct4, and reduced a portion of the CD44highCD24low cell population. celastrol 0-9 CD44 molecule (Indian blood group) Homo sapiens 123-127 30389635-8 2019 To further understand the cancer therapeutic target, we assessed the effect of celastrol on expression of Pin1, which is reportedly overexpressed in many human cancers and activates more than 40 oncogenes or inactivates more than 20 tumor suppressor genes. celastrol 79-88 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 106-110 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 49-53 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 AKT serine/threonine kinase 1 Homo sapiens 85-88 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 signal transducer and activator of transcription 3 Homo sapiens 90-95 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 mitogen-activated protein kinase 14 Homo sapiens 97-100 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 mitogen-activated protein kinase 8 Homo sapiens 102-105 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 RELA proto-oncogene, NF-kB subunit Homo sapiens 107-110 30389635-9 2019 We report that celastrol particularly suppressed Pin1 expression, thereby inhibiting Akt, STAT3, P38, JNK, P65, and IL-6 expression. celastrol 15-24 interleukin 6 Homo sapiens 116-120 30389635-10 2019 Taken together, these findings indicate that celastrol is a potential therapeutic agent for ovarian cancer in humans via inhibition of Pin1 expression. celastrol 45-54 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Homo sapiens 135-139 31113607-0 2019 Celastrol Attenuates Intrahepatic Cholestasis of Pregnancy by Inhibiting Matrix Metalloproteinases-2 and 9. celastrol 0-9 matrix metallopeptidase 2 Rattus norvegicus 73-106 31113607-2 2019 Meanwhile, ample evidences have demonstrated that celastrol inhibits the activity and expression of MMPs. celastrol 50-59 matrix metallopeptidase 2 Homo sapiens 100-104 31113607-6 2019 RESULTS: In rats with ICP, both MMP-2 and -9 exhibited significantly elevated activities, which were inhibited by the administration of celastrol. celastrol 136-145 matrix metallopeptidase 2 Rattus norvegicus 32-44 31113607-9 2019 CONCLUSION: Our findings described for the first time the effects of celastrol to attenuate ICP symptoms through an inhibition of both MMP-2 and -9, providing evidence for a potential role of celastrol as a new drug for the treatment of ICP. celastrol 69-78 matrix metallopeptidase 2 Rattus norvegicus 135-147 31113607-9 2019 CONCLUSION: Our findings described for the first time the effects of celastrol to attenuate ICP symptoms through an inhibition of both MMP-2 and -9, providing evidence for a potential role of celastrol as a new drug for the treatment of ICP. celastrol 192-201 matrix metallopeptidase 2 Rattus norvegicus 135-147 31032752-0 2019 Celastrol Protects RPE Cells from Oxidative Stress-Induced Cell Death via Activation of Nrf2 Signaling Pathway. celastrol 0-9 NFE2 like bZIP transcription factor 2 Homo sapiens 88-92 31032752-11 2019 Treatment with celastrol enhanced the expression of transcription factor Nrf2 and its targets, GCLM and HO-1. celastrol 15-24 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77 31032752-11 2019 Treatment with celastrol enhanced the expression of transcription factor Nrf2 and its targets, GCLM and HO-1. celastrol 15-24 glutamate-cysteine ligase modifier subunit Homo sapiens 95-99 31032752-11 2019 Treatment with celastrol enhanced the expression of transcription factor Nrf2 and its targets, GCLM and HO-1. celastrol 15-24 heme oxygenase 1 Homo sapiens 104-108 31032752-12 2019 Knockdown of Nrf2 expression by shRNA partially abolished the protective effects of celastrol. celastrol 84-93 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 31032752-15 2019 CONCLUSION: This study provides evidence that treatment of RPE cells with celastrol shows potent protective effects against oxidative insults via activation of Nrf2 signaling pathway and upregulation of GCLM expression. celastrol 74-83 NFE2 like bZIP transcription factor 2 Homo sapiens 160-164 31032752-15 2019 CONCLUSION: This study provides evidence that treatment of RPE cells with celastrol shows potent protective effects against oxidative insults via activation of Nrf2 signaling pathway and upregulation of GCLM expression. celastrol 74-83 glutamate-cysteine ligase modifier subunit Homo sapiens 203-207 30472522-5 2019 Celastrol simultaneously reduced the activation of microglia (especially M1 microglia) in the spinal cord, inhibited the pyroptosis-related proteins (NLRP3 ASC Caspase-1 GSDMD), reduced the release of TNF-alpha IL-1beta and IL-18 inflammatory factors, and increased the release of IL10 cytokines. celastrol 0-9 interleukin 10 Rattus norvegicus 281-285 30472522-6 2019 In vitro studies showed that Celastrol reduced the toxicity resulting from the administration of LPS with ATP to BV-2 cells, inhibited the pyroptosis-related proteins (NLRP3 Caspase-1 GSDMD), and inhibited the release of corresponding inflammatory factors. celastrol 29-38 NLR family, pyrin domain containing 3 Mus musculus 168-173 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 BCL2 apoptosis regulator Homo sapiens 83-87 30525586-0 2018 Celastrol Promotes Weight Loss in Diet-Induced Obesity by Inhibiting the Protein Tyrosine Phosphatases PTP1B and TCPTP in the Hypothalamus. celastrol 0-9 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 103-108 30525586-0 2018 Celastrol Promotes Weight Loss in Diet-Induced Obesity by Inhibiting the Protein Tyrosine Phosphatases PTP1B and TCPTP in the Hypothalamus. celastrol 0-9 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 113-118 30525586-2 2018 Celastrol-administered mice at 100 mug/kg decrease food consumption and body weight via a leptin-dependent mechanism, yet its molecular targets in this pathway remain elusive. celastrol 0-9 leptin Mus musculus 90-96 30525586-3 2018 Here, we demonstrate in vivo that celastrol-induced weight loss is largely mediated by the inhibition of leptin negative regulators protein tyrosine phosphatase (PTP) 1B (PTP1B) and T-cell PTP (TCPTP) in the arcuate nucleus (ARC) of the hypothalamus. celastrol 34-43 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 171-176 30525586-3 2018 Here, we demonstrate in vivo that celastrol-induced weight loss is largely mediated by the inhibition of leptin negative regulators protein tyrosine phosphatase (PTP) 1B (PTP1B) and T-cell PTP (TCPTP) in the arcuate nucleus (ARC) of the hypothalamus. celastrol 34-43 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 194-199 30525586-4 2018 We show in vitro that celastrol binds reversibly and inhibits noncompetitively PTP1B and TCPTP. celastrol 22-31 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 79-84 30525586-4 2018 We show in vitro that celastrol binds reversibly and inhibits noncompetitively PTP1B and TCPTP. celastrol 22-31 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 89-94 30525586-6 2018 By using a panel of PTPs implicated in hypothalamic leptin signaling, we show that celastrol additionally inhibited PTEN and SHP2 but had no activity toward other phosphatases of the PTP family. celastrol 83-92 leptin Mus musculus 52-58 30525586-6 2018 By using a panel of PTPs implicated in hypothalamic leptin signaling, we show that celastrol additionally inhibited PTEN and SHP2 but had no activity toward other phosphatases of the PTP family. celastrol 83-92 phosphatase and tensin homolog Mus musculus 116-120 30525586-6 2018 By using a panel of PTPs implicated in hypothalamic leptin signaling, we show that celastrol additionally inhibited PTEN and SHP2 but had no activity toward other phosphatases of the PTP family. celastrol 83-92 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 125-129 30525586-7 2018 These results suggest that PTP1B and TCPTP in the ARC are essential for celastrol"s weight lowering effects in adult obese mice. celastrol 72-81 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 27-32 30525586-7 2018 These results suggest that PTP1B and TCPTP in the ARC are essential for celastrol"s weight lowering effects in adult obese mice. celastrol 72-81 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 37-42 30588010-0 2018 Celastrol induces ubiquitin-dependent degradation of mTOR in breast cancer cells. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 53-57 30588010-2 2018 Celastrol inhibits PI3K-Akt-mTOR signaling, which is frequently dysregulated in tumors and critical for tumor-cell proliferation and survival, but the underlying mechanisms are still not fully understood. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 28-32 30588010-3 2018 In the present study, we investigated detailed mechanisms of celastrol inhibition of mTOR signaling in breast cancer cells. celastrol 61-70 mechanistic target of rapamycin kinase Homo sapiens 85-89 30588010-5 2018 Second, we examined the effects of celastrol on mTOR phosphorylation and expression using Western blot. celastrol 35-44 mechanistic target of rapamycin kinase Homo sapiens 48-52 30588010-6 2018 Furthermore, we investigated the cause of mTOR downregulation by celastrol using immunoprecipitation assays. celastrol 65-74 mechanistic target of rapamycin kinase Homo sapiens 42-46 30588010-9 2018 Celastrol inhibited mTOR phosphorylation and induced mTOR ubiquitination, resulting in its proteasomal degradation. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 20-24 30588010-9 2018 Celastrol inhibited mTOR phosphorylation and induced mTOR ubiquitination, resulting in its proteasomal degradation. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 53-57 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 heat shock protein 90 alpha family class A member 1 Homo sapiens 51-56 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 cell division cycle 37, HSP90 cochaperone Homo sapiens 57-62 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 mechanistic target of rapamycin kinase Homo sapiens 105-109 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 heat shock protein 90 alpha family class A member 1 Homo sapiens 137-142 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 mechanistic target of rapamycin kinase Homo sapiens 105-109 30588010-10 2018 Mechanistically, we found that mTOR is a client of Hsp90-Cdc37 chaperone complex, and celastrol disrupts mTOR interaction with chaperone Hsp90 while promoting mTOR association with cochaperone Cdc37. celastrol 86-95 cell division cycle 37, HSP90 cochaperone Homo sapiens 193-198 30588010-11 2018 Conclusion: Our study reveals that celastrol suppresses mTOR signaling, at least in part through regulating its association with chaperones and inducing its ubiquitination. celastrol 35-44 mechanistic target of rapamycin kinase Homo sapiens 56-60 30316059-0 2018 Discovery of novel NO-releasing celastrol derivatives with Hsp90 inhibition and cytotoxic activities. celastrol 32-41 heat shock protein 90 alpha family class A member 1 Homo sapiens 59-64 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 BCL2 apoptosis regulator Homo sapiens 51-68 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 BCL2 apoptosis regulator Homo sapiens 70-74 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 caspase 3 Homo sapiens 77-86 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 caspase 8 Homo sapiens 88-97 30626478-5 2018 The effects of celastrol on the expression of BAX, B-cell lymphoma 2 (Bcl2), caspase-3, caspase-8, caspase-9 mRNA in A549 cells were detected by real-time quantitative PCR. celastrol 15-24 caspase 9 Homo sapiens 99-108 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 32-41 BCL2 apoptosis regulator Homo sapiens 83-87 30439604-0 2018 Celastrol antagonizes high glucose-evoked podocyte injury, inflammation and insulin resistance by restoring the HO-1-mediated autophagy pathway. celastrol 0-9 insulin Homo sapiens 76-83 30439604-0 2018 Celastrol antagonizes high glucose-evoked podocyte injury, inflammation and insulin resistance by restoring the HO-1-mediated autophagy pathway. celastrol 0-9 heme oxygenase 1 Homo sapiens 112-116 30439604-7 2018 Additionally, HG-elevated high transcripts and secretions of pro-inflammatory cytokines were reversed following celastrol treatment, including IL-1beta, TNF-alpha, IL-6. celastrol 112-121 interleukin 1 beta Homo sapiens 143-151 30439604-7 2018 Additionally, HG-elevated high transcripts and secretions of pro-inflammatory cytokines were reversed following celastrol treatment, including IL-1beta, TNF-alpha, IL-6. celastrol 112-121 tumor necrosis factor Homo sapiens 153-162 30439604-7 2018 Additionally, HG-elevated high transcripts and secretions of pro-inflammatory cytokines were reversed following celastrol treatment, including IL-1beta, TNF-alpha, IL-6. celastrol 112-121 interleukin 6 Homo sapiens 164-168 30439604-8 2018 Simultaneously, the inhibitory effects of HG on insulin-triggered glucose uptake and nephrin expression were overturned after celastrol exposure. celastrol 126-135 insulin Homo sapiens 48-55 30439604-8 2018 Simultaneously, the inhibitory effects of HG on insulin-triggered glucose uptake and nephrin expression were overturned after celastrol exposure. celastrol 126-135 NPHS1 adhesion molecule, nephrin Homo sapiens 85-92 30439604-10 2018 Nevertheless, blocking the autophagy signaling by its antagonist 3-MA muted celastrol-protected against HG-evoked cell injury, inflammation and insulin resistance. celastrol 76-85 insulin Homo sapiens 144-151 30439604-11 2018 Importantly, celastrol enhanced heme oxygenase-1 (HO-1) expression in HG-stimulated podocytes. celastrol 13-22 heme oxygenase 1 Homo sapiens 32-48 30439604-11 2018 Importantly, celastrol enhanced heme oxygenase-1 (HO-1) expression in HG-stimulated podocytes. celastrol 13-22 heme oxygenase 1 Homo sapiens 50-54 30439604-12 2018 Notably, HO-1 cessation depressed autophagy pathway activation and subsequently blunted beneficial effects of celastrol on HG-exposed podocytes. celastrol 110-119 heme oxygenase 1 Homo sapiens 9-13 30439604-13 2018 These finding suggest that celastrol may protect against HG-induced podocyte injury, inflammation and insulin resistance by restoring HO-1-mediated autophagy pathway, implying a promising therapeutic strategy against DN. celastrol 27-36 insulin Homo sapiens 102-109 30439604-13 2018 These finding suggest that celastrol may protect against HG-induced podocyte injury, inflammation and insulin resistance by restoring HO-1-mediated autophagy pathway, implying a promising therapeutic strategy against DN. celastrol 27-36 heme oxygenase 1 Homo sapiens 134-138 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 caspase 8 Homo sapiens 212-221 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 caspase 9 Homo sapiens 223-232 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 caspase 3 Homo sapiens 236-245 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 caspase 8 Homo sapiens 249-258 30626478-8 2018 Compared with the group without celastrol treatment, the mRNA and protein level of Bcl2 in A549 cells treated with (1, 3) mumol/L celastrol decreased significantly, while the expression levels of BAX, caspase-3, caspase-8, caspase-9, c-caspase-3, c-caspase-8, c-caspase-9 increased significantly. celastrol 130-139 caspase 9 Homo sapiens 262-271 30333251-0 2018 Systematic identification of Celastrol-binding proteins reveals that Shoc2 is inhibited by Celastrol. celastrol 29-38 SHOC2 leucine rich repeat scaffold protein Homo sapiens 69-74 30333251-0 2018 Systematic identification of Celastrol-binding proteins reveals that Shoc2 is inhibited by Celastrol. celastrol 91-100 SHOC2 leucine rich repeat scaffold protein Homo sapiens 69-74 30333251-8 2018 Celastrol significantly inhibited ERK1/2 phosphorylation in cell lines and xenograft tumors. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 34-40 30333251-12 2018 In summary, we unraveled the anti-CRC function of Celastrol and confirmed for the first time that it inhibited the ERK1/2 pathway through binding to Shoc2. celastrol 50-59 mitogen-activated protein kinase 3 Homo sapiens 115-121 30333251-12 2018 In summary, we unraveled the anti-CRC function of Celastrol and confirmed for the first time that it inhibited the ERK1/2 pathway through binding to Shoc2. celastrol 50-59 SHOC2 leucine rich repeat scaffold protein Homo sapiens 149-154 29355035-0 2018 Simultaneous targeting therapy for lung metastasis and breast tumor by blocking the NF-kappaB signaling pathway using Celastrol-loaded micelles. celastrol 118-127 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 84-93 30510417-1 2018 Purpose: A transferrin-modified microemulsion carrying coix seed oil and tripterine (Tf-CT-MEs) was developed for improved tumor-specific accumulation and penetration to enhance cervical cancer treatment. celastrol 73-83 transferrin Homo sapiens 11-22 30158241-0 2018 Celastrol-Induced Weight Loss Is Driven by Hypophagia and Independent From UCP1. celastrol 0-9 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 75-79 30158241-5 2018 Protein tyrosine phosphatase 1 (PTP1B), a leptin negative-feedback regulator, has been previously reported to be one of celastrol"s targets. celastrol 120-129 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 32-37 30158241-6 2018 However, we found that global PTP1B knockout (KO) and wild-type (WT) mice have comparable weight loss and hypophagia when treated with celastrol. celastrol 135-144 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 30-35 30158241-7 2018 Increased levels of uncoupling protein 1 (UCP1) in subcutaneous white and brown adipose tissue suggest celastrol-induced thermogenesis as a further mechanism. celastrol 103-112 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 20-40 30158241-7 2018 Increased levels of uncoupling protein 1 (UCP1) in subcutaneous white and brown adipose tissue suggest celastrol-induced thermogenesis as a further mechanism. celastrol 103-112 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 42-46 30498444-0 2018 Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway. celastrol 0-9 endothelin receptor type B Mus musculus 130-135 30498444-0 2018 Celastrol Alleviates Chronic Obstructive Pulmonary Disease by Inhibiting Cellular Inflammation Induced by Cigarette Smoke via the Ednrb/Kng1 Signaling Pathway. celastrol 0-9 kininogen 1 Mus musculus 136-140 30498444-13 2018 Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor alpha and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. celastrol 54-63 chemokine (C-X-C motif) ligand 15 Mus musculus 123-136 30498444-13 2018 Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor alpha and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. celastrol 54-63 tumor necrosis factor Mus musculus 138-165 30498444-13 2018 Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor alpha and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. celastrol 54-63 chemokine (C-C motif) ligand 2 Mus musculus 170-204 30498444-13 2018 Compared to mice in the COPD group, mice treated with Celastrol had significantly reduced levels of inflammatory cytokines interleukin-8, tumor necrosis factor alpha and monocyte chemoattractant protein-1 in the serum and bronchoalveolar lavage fluid, and significantly increased levels of oxidative stress factors superoxide dismutase and catalase. celastrol 54-63 catalase Mus musculus 340-348 30498444-18 2018 Additionally, Celastrol effectively reduced Ednrb/Kng1 expression in both cell and animal models. celastrol 14-23 endothelin receptor type B Mus musculus 44-49 30498444-18 2018 Additionally, Celastrol effectively reduced Ednrb/Kng1 expression in both cell and animal models. celastrol 14-23 kininogen 1 Mus musculus 50-54 30498444-19 2018 Celastrol has a therapeutic effect on COPD and may alleviate COPD by inhibiting inflammation development by suppressing the Ednrb/Kng1 signaling pathway. celastrol 0-9 endothelin receptor type B Mus musculus 124-129 30498444-19 2018 Celastrol has a therapeutic effect on COPD and may alleviate COPD by inhibiting inflammation development by suppressing the Ednrb/Kng1 signaling pathway. celastrol 0-9 kininogen 1 Mus musculus 130-134 29355035-2 2018 To inhibit the metastasis and growth of breast tumor simultaneously, a Celastrol (Cela) loaded glucolipid-like conjugates (CSOSA/Cela) with alphavbeta3-ligand Tetraiodothyroacetic acid (TET) modification (TET-CSOSA/Cela) were established to block nuclear factor-kappa B (NF-kappaB) signaling pathway. celastrol 71-80 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 247-269 29355035-2 2018 To inhibit the metastasis and growth of breast tumor simultaneously, a Celastrol (Cela) loaded glucolipid-like conjugates (CSOSA/Cela) with alphavbeta3-ligand Tetraiodothyroacetic acid (TET) modification (TET-CSOSA/Cela) were established to block nuclear factor-kappa B (NF-kappaB) signaling pathway. celastrol 71-80 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 271-280 29355035-2 2018 To inhibit the metastasis and growth of breast tumor simultaneously, a Celastrol (Cela) loaded glucolipid-like conjugates (CSOSA/Cela) with alphavbeta3-ligand Tetraiodothyroacetic acid (TET) modification (TET-CSOSA/Cela) were established to block nuclear factor-kappa B (NF-kappaB) signaling pathway. celastrol 71-75 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 247-269 29355035-2 2018 To inhibit the metastasis and growth of breast tumor simultaneously, a Celastrol (Cela) loaded glucolipid-like conjugates (CSOSA/Cela) with alphavbeta3-ligand Tetraiodothyroacetic acid (TET) modification (TET-CSOSA/Cela) were established to block nuclear factor-kappa B (NF-kappaB) signaling pathway. celastrol 71-75 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 271-280 29355035-4 2018 The results demonstrated that TET-CSOSA/Cela significantly suppressed Bcl-2 activation of lung metastatic cells and reduced MMP-9 expression of 4T1 breast tumor cells by blocking NF-kappaB. celastrol 40-44 B cell leukemia/lymphoma 2 Mus musculus 70-75 29355035-4 2018 The results demonstrated that TET-CSOSA/Cela significantly suppressed Bcl-2 activation of lung metastatic cells and reduced MMP-9 expression of 4T1 breast tumor cells by blocking NF-kappaB. celastrol 40-44 matrix metallopeptidase 9 Mus musculus 124-129 29355035-4 2018 The results demonstrated that TET-CSOSA/Cela significantly suppressed Bcl-2 activation of lung metastatic cells and reduced MMP-9 expression of 4T1 breast tumor cells by blocking NF-kappaB. celastrol 40-44 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 179-188 30268856-4 2018 KEY FINDINGS: Pkd1 miRNA transgenic (Pkd1 miR TG) mice treated with 1 mg/kg/day of celastrol exhibited a lower renal cystic index (by 21.5%) than the vehicle-treated controls, but the fractional kidney weights and blood urea nitrogen levels were not significantly affected with celastrol treatment. celastrol 83-92 polycystin 1, transient receptor potential channel interacting Mus musculus 14-18 30221712-0 2018 Celastrol inhibits glucocorticoid-induced osteoporosis in rat via the PI3K/AKT and Wnt signaling pathways. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 75-78 30221712-3 2018 The findings of the current study revealed that Celastrol reduced body weight, urine calcium/creatinine, tartrate-resistant acid phosphatase 5b, C-terminal telopeptide of type I collagen, and induced osteocalcin in GIOP rats. celastrol 48-57 bone gamma-carboxyglutamate protein Rattus norvegicus 200-211 30221712-5 2018 Celastrol inhibited prostaglandin E2 and caspase-3 protein expression levels, and induced phosphoinositol 3-kinase (PI3K), phosphorylated-protein kinase B (AKT) and glycogen synthase kinase-3 phosphorylation, Wnt and beta-catenin protein expression in GIOP rats. celastrol 0-9 caspase 3 Rattus norvegicus 41-50 30221712-5 2018 Celastrol inhibited prostaglandin E2 and caspase-3 protein expression levels, and induced phosphoinositol 3-kinase (PI3K), phosphorylated-protein kinase B (AKT) and glycogen synthase kinase-3 phosphorylation, Wnt and beta-catenin protein expression in GIOP rats. celastrol 0-9 phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit beta Rattus norvegicus 90-114 30221712-5 2018 Celastrol inhibited prostaglandin E2 and caspase-3 protein expression levels, and induced phosphoinositol 3-kinase (PI3K), phosphorylated-protein kinase B (AKT) and glycogen synthase kinase-3 phosphorylation, Wnt and beta-catenin protein expression in GIOP rats. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 156-159 30221712-5 2018 Celastrol inhibited prostaglandin E2 and caspase-3 protein expression levels, and induced phosphoinositol 3-kinase (PI3K), phosphorylated-protein kinase B (AKT) and glycogen synthase kinase-3 phosphorylation, Wnt and beta-catenin protein expression in GIOP rats. celastrol 0-9 catenin beta 1 Rattus norvegicus 217-229 30221712-6 2018 The present study demonstrated that Celastrol may inhibit GIOP in rats via the PI3K/AKT and Wnt signaling pathways. celastrol 36-45 AKT serine/threonine kinase 1 Rattus norvegicus 84-87 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 polycystin 1, transient receptor potential channel interacting Mus musculus 217-221 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 microRNA 615 Mus musculus 222-225 30268856-4 2018 KEY FINDINGS: Pkd1 miRNA transgenic (Pkd1 miR TG) mice treated with 1 mg/kg/day of celastrol exhibited a lower renal cystic index (by 21.5%) than the vehicle-treated controls, but the fractional kidney weights and blood urea nitrogen levels were not significantly affected with celastrol treatment. celastrol 83-92 polycystin 1, transient receptor potential channel interacting Mus musculus 37-41 30268856-4 2018 KEY FINDINGS: Pkd1 miRNA transgenic (Pkd1 miR TG) mice treated with 1 mg/kg/day of celastrol exhibited a lower renal cystic index (by 21.5%) than the vehicle-treated controls, but the fractional kidney weights and blood urea nitrogen levels were not significantly affected with celastrol treatment. celastrol 83-92 microRNA 615 Mus musculus 19-22 30268856-4 2018 KEY FINDINGS: Pkd1 miRNA transgenic (Pkd1 miR TG) mice treated with 1 mg/kg/day of celastrol exhibited a lower renal cystic index (by 21.5%) than the vehicle-treated controls, but the fractional kidney weights and blood urea nitrogen levels were not significantly affected with celastrol treatment. celastrol 278-287 polycystin 1, transient receptor potential channel interacting Mus musculus 14-18 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 tumor necrosis factor Mus musculus 64-91 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 interleukin 1 beta Mus musculus 93-110 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 112-117 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 adhesion G protein-coupled receptor E1 Mus musculus 119-124 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 CD68 antigen Mus musculus 126-130 30268856-7 2018 Moreover, celastrol reduced the renal mRNA expression levels of tumor necrosis factor-alpha, interleukin-1beta, P2RX7, F4/80, CD68, transforming growth factor-beta, collagen-1, and fibronectin, which were high in the Pkd1 miR TG mice. celastrol 10-19 fibronectin 1 Mus musculus 181-192 29667734-6 2018 Bioinformatics and cellular experiments showed that both celastrol and PA could bind MD2, and that celastrol could expel PA from cells. celastrol 57-66 lymphocyte antigen 96 Homo sapiens 85-88 30015859-0 2018 Effect of celastrol on toll-like receptor 4-mediated inflammatory response in free fatty acid-induced HepG2 cells. celastrol 10-19 toll like receptor 4 Homo sapiens 23-43 30015859-2 2018 Our previous study demonstrated that celastrol treatment was able to improve hepatic steatosis and inhibit the TLR4 signaling cascade pathway in type 2 diabetic rats. celastrol 37-46 toll-like receptor 4 Rattus norvegicus 111-115 30015859-6 2018 To directly elucidate whether TLR4 was the blocking target of celastrol upon FFA exposure, the cellular response to inflammation was determined upon transfection with TLR4 siRNA. celastrol 62-71 toll like receptor 4 Homo sapiens 30-34 30015859-7 2018 The results revealed that celastrol significantly reduced triglyceride accumulation in the steatotic HepG2 cells, and downregulated the expression levels of TLR4, MyD88 and phospho-NF-kappaBp65, as well as of the downstream inflammatory cytokines interleukin-1beta and tumor necrosis factor alpha. celastrol 26-35 toll like receptor 4 Homo sapiens 157-161 30015859-7 2018 The results revealed that celastrol significantly reduced triglyceride accumulation in the steatotic HepG2 cells, and downregulated the expression levels of TLR4, MyD88 and phospho-NF-kappaBp65, as well as of the downstream inflammatory cytokines interleukin-1beta and tumor necrosis factor alpha. celastrol 26-35 MYD88 innate immune signal transduction adaptor Homo sapiens 163-168 30015859-7 2018 The results revealed that celastrol significantly reduced triglyceride accumulation in the steatotic HepG2 cells, and downregulated the expression levels of TLR4, MyD88 and phospho-NF-kappaBp65, as well as of the downstream inflammatory cytokines interleukin-1beta and tumor necrosis factor alpha. celastrol 26-35 interleukin 1 beta Homo sapiens 247-296 29873512-10 2018 Another drug, celastrol, which enhanced expression of ER and cytosolic chaperones in GECs, tended to reduce actinin-4 aggregation but did not decrease the tight association of actinin-4 K256E with F-actin and did not reduce albuminuria in actinin-4 K256E transgenic mice. celastrol 14-23 actinin alpha 4 Mus musculus 108-117 30268831-7 2018 FINDINGS: In vivo, after celastrol treatment, cisplatin-induced kidney injury was significantly ameliorated as shown by the improvement of renal function (BUN, serum creatinine, and cystatin C), kidney morphology (PAS staining) and oxidative stress (MDA) and the suppression of renal tubular injury markers of KIM-1 and NGAL. celastrol 25-34 cystatin C Mus musculus 182-192 30268831-7 2018 FINDINGS: In vivo, after celastrol treatment, cisplatin-induced kidney injury was significantly ameliorated as shown by the improvement of renal function (BUN, serum creatinine, and cystatin C), kidney morphology (PAS staining) and oxidative stress (MDA) and the suppression of renal tubular injury markers of KIM-1 and NGAL. celastrol 25-34 hepatitis A virus cellular receptor 1 Mus musculus 310-315 29667734-0 2018 Celastrol reverses palmitic acid (PA)-caused TLR4-MD2 activation-dependent insulin resistance via disrupting MD2-related cellular binding to PA. celastrol 0-9 toll like receptor 4 Homo sapiens 45-49 29667734-0 2018 Celastrol reverses palmitic acid (PA)-caused TLR4-MD2 activation-dependent insulin resistance via disrupting MD2-related cellular binding to PA. celastrol 0-9 lymphocyte antigen 96 Homo sapiens 50-53 29667734-0 2018 Celastrol reverses palmitic acid (PA)-caused TLR4-MD2 activation-dependent insulin resistance via disrupting MD2-related cellular binding to PA. celastrol 0-9 insulin Homo sapiens 75-82 29667734-0 2018 Celastrol reverses palmitic acid (PA)-caused TLR4-MD2 activation-dependent insulin resistance via disrupting MD2-related cellular binding to PA. celastrol 0-9 lymphocyte antigen 96 Homo sapiens 109-112 29667734-8 2018 Taking together, we proved that celastrol could reverses PA-caused TLR4-MD2 activation-dependent insulin resistance via disrupting PA binding to MD2. celastrol 32-41 toll like receptor 4 Homo sapiens 67-71 29667734-8 2018 Taking together, we proved that celastrol could reverses PA-caused TLR4-MD2 activation-dependent insulin resistance via disrupting PA binding to MD2. celastrol 32-41 lymphocyte antigen 96 Homo sapiens 72-75 29667734-8 2018 Taking together, we proved that celastrol could reverses PA-caused TLR4-MD2 activation-dependent insulin resistance via disrupting PA binding to MD2. celastrol 32-41 insulin Homo sapiens 97-104 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 3-12 lymphocyte antigen 96 Homo sapiens 44-47 29667734-8 2018 Taking together, we proved that celastrol could reverses PA-caused TLR4-MD2 activation-dependent insulin resistance via disrupting PA binding to MD2. celastrol 32-41 lymphocyte antigen 96 Homo sapiens 145-148 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 3-12 lymphocyte antigen 96 Homo sapiens 100-103 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 133-142 lymphocyte antigen 96 Homo sapiens 44-47 30255683-6 2018 With the increase of the concentration of celastrol, the ratio of Bax/Bcl-2 protein was up-regulated. celastrol 42-51 BCL2 associated X, apoptosis regulator Homo sapiens 66-69 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 133-142 lymphocyte antigen 96 Homo sapiens 100-103 29667734-4 2018 As celastrol is reported to directly target MD2, we thought disrupting the binding between FFAs and MD2 might be one of the ways for celastrol to inhibit FFAs-caused inflammation and insulin resistance. celastrol 133-142 insulin Homo sapiens 183-190 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 toll like receptor 4 Homo sapiens 94-98 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 lymphocyte antigen 96 Homo sapiens 99-102 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 insulin Homo sapiens 124-131 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 insulin Homo sapiens 212-219 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 toll like receptor 4 Homo sapiens 248-252 29667734-5 2018 In this study, we found evidence to support our hypothesis: celastrol could reverse PA-caused TLR4/MD2 activation-dependent insulin resistance, as determined by glucose-lowering ability, cellular glucose uptake, insulin action-related proteins and TLR4/MD2/NF-kappaB activation. celastrol 60-69 lymphocyte antigen 96 Homo sapiens 253-256 30106429-7 2018 Pretreatment with the PERK inhibitor GSK2656157 significantly promoted celastrol-induced death and attenuated HOS cell autophagy. celastrol 71-80 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 22-26 30106429-9 2018 The ERS/PERK pathway may protect HOS cells from apoptosis by celastrol and may play a complicated role in the process of autophagy. celastrol 61-70 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 8-12 30015859-10 2018 These results suggest that celastrol exerts its protective effect partly via inhibiting the TLR4-mediated immune and inflammatory response in steatotic HepG2 cells. celastrol 27-36 toll like receptor 4 Homo sapiens 92-96 30255683-6 2018 With the increase of the concentration of celastrol, the ratio of Bax/Bcl-2 protein was up-regulated. celastrol 42-51 BCL2 apoptosis regulator Homo sapiens 70-75 30255683-7 2018 The Caspase-3/7 protein was cleaved and activated after treatment with celastrol. celastrol 71-80 caspase 3 Homo sapiens 4-15 30255683-9 2018 Taken together, these results indicated that celastrol effectively inhibited the proliferation of adult T-cell leukemia cells by regulating the expression of Bcl-2 family protein, and induced cell apoptosis by activating Caspase dependent pathway. celastrol 45-54 BCL2 apoptosis regulator Homo sapiens 158-163 30103947-4 2018 We found that celastrol, a c-Myb inhibitor, inhibited NK-92 cells more strongly than any other inhibitors of transcription factor candidates. celastrol 14-23 MYB proto-oncogene, transcription factor Homo sapiens 27-32 30093405-6 2018 Pharmacological up-regulation of Hsp70 by the Hsp90 inhibitors celastrol and herbimycin A attenuated the aggregation of mutant PKCgamma in primary cultured Purkinje cells. celastrol 63-72 heat shock protein, 2 Mus musculus 46-51 30093405-6 2018 Pharmacological up-regulation of Hsp70 by the Hsp90 inhibitors celastrol and herbimycin A attenuated the aggregation of mutant PKCgamma in primary cultured Purkinje cells. celastrol 63-72 protein kinase C, gamma Mus musculus 127-135 30093405-9 2018 Extending our in vitro observations, administration of celastrol to mice up-regulated cerebellar Hsp70. celastrol 55-64 heat shock protein 1B Mus musculus 97-102 30093405-6 2018 Pharmacological up-regulation of Hsp70 by the Hsp90 inhibitors celastrol and herbimycin A attenuated the aggregation of mutant PKCgamma in primary cultured Purkinje cells. celastrol 63-72 heat shock protein 1B Mus musculus 33-38 30103947-6 2018 We also found that celastrol inhibits NK-92-cell-mediated cytotoxicity via the downregulation of NKG2D and granzyme B. celastrol 19-28 killer cell lectin like receptor K1 Homo sapiens 97-102 30103947-6 2018 We also found that celastrol inhibits NK-92-cell-mediated cytotoxicity via the downregulation of NKG2D and granzyme B. celastrol 19-28 granzyme B Homo sapiens 107-117 30839692-8 2018 Furthermore, it was confirmed that celastrol, a positive drug for the treatment of RA, inhibited SW982 cell migration as well as TRAP activity in the cell-cultured microfluidic chips. celastrol 35-44 acid phosphatase 5, tartrate resistant Mus musculus 129-133 29913408-9 2018 Tripterine alleviated LPS-induced reduction of cell viability, increase of apoptosis and the release of IL-6 and TNF-alpha in HaCaT cells. celastrol 0-10 tumor necrosis factor Homo sapiens 113-122 29927769-0 2018 Celastrol improves the therapeutic efficacy of EGFR-TKIs for non-small-cell lung cancer by overcoming EGFR T790M drug resistance. celastrol 0-9 epidermal growth factor receptor Homo sapiens 47-51 29927769-0 2018 Celastrol improves the therapeutic efficacy of EGFR-TKIs for non-small-cell lung cancer by overcoming EGFR T790M drug resistance. celastrol 0-9 epidermal growth factor receptor Homo sapiens 102-106 29927769-5 2018 In this study, we showed that celastrol combined with EGFR-TKIs significantly suppressed cell invasion of lung cancer cells with a T790M mutation by suppressing the EGFR pathway. celastrol 30-39 epidermal growth factor receptor Homo sapiens 165-169 29927769-7 2018 Together, these results suggested that combined therapy with EGFR-TKIs and celastrol may be a more effective treatment of patients with non-small-cell lung cancer with T790M mutations of the EGFR. celastrol 75-84 epidermal growth factor receptor Homo sapiens 191-195 29913408-0 2018 Tripterine alleviates LPS-induced inflammatory injury by up-regulation of miR-146a in HaCaT cells. celastrol 0-10 microRNA 146a Homo sapiens 74-82 29913408-9 2018 Tripterine alleviated LPS-induced reduction of cell viability, increase of apoptosis and the release of IL-6 and TNF-alpha in HaCaT cells. celastrol 0-10 interleukin 6 Homo sapiens 104-108 29614269-3 2018 Here, we found that celastrol dose-dependently suppressed IL-13 induced CD206 expression both in RAW264.7 and in primary macrophages. celastrol 20-29 interleukin 13 Homo sapiens 58-63 29614269-3 2018 Here, we found that celastrol dose-dependently suppressed IL-13 induced CD206 expression both in RAW264.7 and in primary macrophages. celastrol 20-29 mannose receptor C-type 1 Homo sapiens 72-77 29614269-4 2018 Consistently, celastrol also inhibited the expression of M2-like specific genes, including MRC1, Arg1, Fizz1, Mgl2 and CD11c. celastrol 14-23 mannose receptor C-type 1 Homo sapiens 91-95 29614269-4 2018 Consistently, celastrol also inhibited the expression of M2-like specific genes, including MRC1, Arg1, Fizz1, Mgl2 and CD11c. celastrol 14-23 arginase 1 Homo sapiens 97-101 29614269-4 2018 Consistently, celastrol also inhibited the expression of M2-like specific genes, including MRC1, Arg1, Fizz1, Mgl2 and CD11c. celastrol 14-23 resistin like beta Homo sapiens 103-108 29614269-4 2018 Consistently, celastrol also inhibited the expression of M2-like specific genes, including MRC1, Arg1, Fizz1, Mgl2 and CD11c. celastrol 14-23 integrin subunit alpha X Homo sapiens 119-124 29614269-6 2018 Mechanistically, celastrol completely ameliorated STAT6 phosphorylation, which is the key signal molecule responsible for M2 polarization. celastrol 17-26 signal transducer and activator of transcription 6 Homo sapiens 50-55 29614269-7 2018 Our research puts forward a new application of celastrol in anti-cancer metastasis, by intervening M2-like polarization through inhibiting STAT6. celastrol 47-56 signal transducer and activator of transcription 6 Homo sapiens 139-144 29913408-11 2018 Further, inhibition of miR-146a abolished the protective effect of tripterine on cell damage triggered by LPS. celastrol 67-77 microRNA 146a Homo sapiens 23-31 29913408-12 2018 Finally, tripterine deactivated JNK and NF-kappaB pathways through up-regulation of miR-146a. celastrol 9-19 mitogen-activated protein kinase 8 Homo sapiens 32-35 29913408-12 2018 Finally, tripterine deactivated JNK and NF-kappaB pathways through up-regulation of miR-146a. celastrol 9-19 microRNA 146a Homo sapiens 84-92 29913408-13 2018 CONCLUSION: These results demonstrated that tripterine could attenuate LPS-induced inflammatory injury and deactivate JNK and NF-kappaB pathways by up-regulation of miR-146a. celastrol 44-54 mitogen-activated protein kinase 8 Homo sapiens 118-121 29913408-13 2018 CONCLUSION: These results demonstrated that tripterine could attenuate LPS-induced inflammatory injury and deactivate JNK and NF-kappaB pathways by up-regulation of miR-146a. celastrol 44-54 microRNA 146a Homo sapiens 165-173 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 296 Rattus norvegicus 73-80 30220146-0 2018 [Influence of celastrol on toll-like receptor 4-mediated signaling pathway in the free fatty acids-induced HepG2 cells]. celastrol 14-23 toll like receptor 4 Homo sapiens 27-47 30220146-10 2018 Conclusion: Celastrol exerts its protective effect partly via inhibiting the TLR4-mediated signaling pathways in the steatotic HepG2 cells. celastrol 12-21 toll like receptor 4 Homo sapiens 77-81 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 22 Rattus norvegicus 26-32 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 27a Rattus norvegicus 34-41 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 96 Rattus norvegicus 43-49 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 142 Rattus norvegicus 51-58 30081592-7 2018 Interestingly, 6 of them (miR-22, miR-27a, miR-96, miR-142, miR-223, and miR-296) were further modulated by celastrol treatment. celastrol 108-117 microRNA 223 Rattus norvegicus 60-67 30081592-8 2018 Interestingly, serum levels of miR-142, miR-155, and miR-223 were higher in arthritic versus control rats, whereas miR-212 showed increased expression in celastrol-treated rats compared with arthritic rats or control rats. celastrol 154-163 microRNA 212 Rattus norvegicus 115-122 29631379-10 2018 Furthermore, treatment of Caco-2 cells with celastrol (NF-kappaB inhibitor) blocked the inhibitory effect caused by TNF-alpha on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. celastrol 44-53 nuclear factor kappa B subunit 1 Homo sapiens 55-64 29631379-10 2018 Furthermore, treatment of Caco-2 cells with celastrol (NF-kappaB inhibitor) blocked the inhibitory effect caused by TNF-alpha on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. celastrol 44-53 tumor necrosis factor Homo sapiens 116-125 29631379-10 2018 Furthermore, treatment of Caco-2 cells with celastrol (NF-kappaB inhibitor) blocked the inhibitory effect caused by TNF-alpha on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. celastrol 44-53 solute carrier family 23 member 1 Homo sapiens 140-146 29631379-10 2018 Furthermore, treatment of Caco-2 cells with celastrol (NF-kappaB inhibitor) blocked the inhibitory effect caused by TNF-alpha on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. celastrol 44-53 solute carrier family 23 member 1 Homo sapiens 204-211 29631379-11 2018 Treatment of TNF-alpha also led to a significant decrease in the expression of hepatocyte nuclear factor-1-alpha, which drives the basal activity of SLC23A1 promoter, and this effect was reversed by celastrol. celastrol 199-208 tumor necrosis factor Homo sapiens 13-22 29631379-11 2018 Treatment of TNF-alpha also led to a significant decrease in the expression of hepatocyte nuclear factor-1-alpha, which drives the basal activity of SLC23A1 promoter, and this effect was reversed by celastrol. celastrol 199-208 HNF1 homeobox A Homo sapiens 79-112 29631379-11 2018 Treatment of TNF-alpha also led to a significant decrease in the expression of hepatocyte nuclear factor-1-alpha, which drives the basal activity of SLC23A1 promoter, and this effect was reversed by celastrol. celastrol 199-208 solute carrier family 23 member 1 Homo sapiens 149-156 29987023-8 2018 Finally, high-throughput screening demonstrated that celastrol, an antioxidant and antiinflammatory agent, reduced the expressions of CyPA and Bsg in the heart and the lung, ameliorating cardiac dysfunction and postcapillary PH induced by TAC. celastrol 53-62 peptidylprolyl isomerase A Mus musculus 134-138 29394529-13 2018 Celastrol reverts these cellular changes in rat lungs, and it was found that celastrol regulates EMT through the inhibition of heat shock protein 90 (HSP 90). celastrol 77-86 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 127-148 29394529-13 2018 Celastrol reverts these cellular changes in rat lungs, and it was found that celastrol regulates EMT through the inhibition of heat shock protein 90 (HSP 90). celastrol 77-86 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 150-156 29987023-8 2018 Finally, high-throughput screening demonstrated that celastrol, an antioxidant and antiinflammatory agent, reduced the expressions of CyPA and Bsg in the heart and the lung, ameliorating cardiac dysfunction and postcapillary PH induced by TAC. celastrol 53-62 basigin Mus musculus 143-146 29987023-9 2018 Thus, by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload HF with postcapillary PH, for which celastrol may be a promising agent. celastrol 166-175 peptidylprolyl isomerase A Mus musculus 34-38 29987023-9 2018 Thus, by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload HF with postcapillary PH, for which celastrol may be a promising agent. celastrol 166-175 basigin Mus musculus 43-46 29987023-9 2018 Thus, by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload HF with postcapillary PH, for which celastrol may be a promising agent. celastrol 166-175 Rho-associated coiled-coil containing protein kinase 1 Mus musculus 60-65 29987023-9 2018 Thus, by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload HF with postcapillary PH, for which celastrol may be a promising agent. celastrol 166-175 Rho-associated coiled-coil containing protein kinase 2 Mus musculus 79-84 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 interleukin 6 Mus musculus 153-157 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 interleukin 1 beta Mus musculus 159-167 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 intercellular adhesion molecule 1 Mus musculus 198-204 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 tumor necrosis factor Mus musculus 169-178 30093945-8 2018 The serum levels of ALT, AST, and LDH were further increased in parallel with the deteriorated liver morphological damage (H&E) and oxidative stress in celastrol-treated mice, indicating an aggravated liver injury. celastrol 156-165 glutamic pyruvic transaminase, soluble Mus musculus 20-23 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 interleukin 18 Mus musculus 180-185 30093945-8 2018 The serum levels of ALT, AST, and LDH were further increased in parallel with the deteriorated liver morphological damage (H&E) and oxidative stress in celastrol-treated mice, indicating an aggravated liver injury. celastrol 156-165 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 25-28 30093945-9 2018 In kidney, the expressions of tubular injury markers of kidney injury molecule-1 (KIM-1) and gelatinase-associated lipocalin (NGAL) were further upregulated along with higher levels of blood urea nitrogen (BUN), creatinine (Cr), and MDA in celastrol-treated mice. celastrol 240-249 hepatitis A virus cellular receptor 1 Mus musculus 56-80 30093945-9 2018 In kidney, the expressions of tubular injury markers of kidney injury molecule-1 (KIM-1) and gelatinase-associated lipocalin (NGAL) were further upregulated along with higher levels of blood urea nitrogen (BUN), creatinine (Cr), and MDA in celastrol-treated mice. celastrol 240-249 hepatitis A virus cellular receptor 1 Mus musculus 82-87 30093945-7 2018 Following celastrol pretreatment, mice showed increased mortality rate and aggravated inflammation evidenced by further enhanced inflammatory markers of IL-6, IL-1beta, TNF-alpha, IL-18, MCP-1, and ICAM-1 in circulation, liver, and kidney after LPS treatment. celastrol 10-19 mast cell protease 1 Mus musculus 187-192 29553945-5 2018 Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. celastrol 0-9 matrix metallopeptidase 7 Homo sapiens 81-85 29553945-0 2018 Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 0-9 matrix metallopeptidase 3 Homo sapiens 93-97 29694830-0 2018 Celastrol attenuates symptoms of preeclampsia in rats by inhibiting matrix metalloproteinase-9. celastrol 0-9 matrix metallopeptidase 9 Rattus norvegicus 68-94 29553945-6 2018 In addition, knockdown of AKT, not mTOR, inhibited MMP3 and MMP7 expression levels and AKT silencing promoted the celastrol-induced effects on CRC cell proliferation and migration. celastrol 114-123 AKT serine/threonine kinase 1 Homo sapiens 87-90 29553945-0 2018 Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 0-9 matrix metallopeptidase 7 Homo sapiens 102-106 29553945-0 2018 Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 119-122 29553945-5 2018 Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 44-47 29553945-7 2018 Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 50-59 matrix metallopeptidase 3 Homo sapiens 108-112 29553945-5 2018 Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. celastrol 0-9 matrix metallopeptidase 3 Homo sapiens 72-76 29553945-7 2018 Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 50-59 matrix metallopeptidase 7 Homo sapiens 117-121 29553945-7 2018 Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway. celastrol 50-59 AKT serine/threonine kinase 1 Homo sapiens 134-137 29493374-4 2018 OBJECTIVE: This study investigated the effect of celastrol on mRNA expression and concentration levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL6) that are induced by influenza A/Puerto Rico/8/34 (H1N1; PR8) in Madin-Darby Canine Kidney (MDCK) cells. celastrol 49-58 tumor necrosis factor Homo sapiens 166-174 29793976-5 2018 Application of a pan-Nox inhibitor, celastrol, during the time of optic nerve (ON) outgrowth resulted in significant expansion of the ganglion cell layer (GCL), thinning of the ON, and a decrease in retinal axons reaching the optic tectum (OT). celastrol 36-45 germ cell-less, spermatogenesis associated Danio rerio 155-158 29694830-9 2018 Urinary mRNA levels of podocin and nephrin, as well as PlGF, MMP-9 and sFlt-1, were all reversed in preeclampsia plus celastrol group compared to rats in the preeclampsia group without celastrol treatments. celastrol 118-127 NPHS2 stomatin family member, podocin Rattus norvegicus 23-30 29694830-9 2018 Urinary mRNA levels of podocin and nephrin, as well as PlGF, MMP-9 and sFlt-1, were all reversed in preeclampsia plus celastrol group compared to rats in the preeclampsia group without celastrol treatments. celastrol 118-127 NPHS1 adhesion molecule, nephrin Rattus norvegicus 35-42 29694830-9 2018 Urinary mRNA levels of podocin and nephrin, as well as PlGF, MMP-9 and sFlt-1, were all reversed in preeclampsia plus celastrol group compared to rats in the preeclampsia group without celastrol treatments. celastrol 118-127 placental growth factor Rattus norvegicus 55-59 29694830-9 2018 Urinary mRNA levels of podocin and nephrin, as well as PlGF, MMP-9 and sFlt-1, were all reversed in preeclampsia plus celastrol group compared to rats in the preeclampsia group without celastrol treatments. celastrol 118-127 matrix metallopeptidase 9 Rattus norvegicus 61-66 29694830-10 2018 MMP-9 overexpression in rats completely abolished the alleviating effect of celastrol. celastrol 76-85 matrix metallopeptidase 9 Rattus norvegicus 0-5 29694830-11 2018 We hereby presented the first evidence that celastrol attenuated preeclampsia symptoms in an L-NAME-induced rat model of preeclampsia through inhibition of MMP-9 expression, supporting the potential therapeutic value of celastrol in the treatment of preeclampsia. celastrol 44-53 matrix metallopeptidase 9 Rattus norvegicus 156-161 29694830-11 2018 We hereby presented the first evidence that celastrol attenuated preeclampsia symptoms in an L-NAME-induced rat model of preeclampsia through inhibition of MMP-9 expression, supporting the potential therapeutic value of celastrol in the treatment of preeclampsia. celastrol 220-229 matrix metallopeptidase 9 Rattus norvegicus 156-161 28984147-7 2018 Also, celastrol posttreatments attenuated the APAP-induced oxidative stress by raising glutathione peroxidase, glutathione reductase, and catalase activities. celastrol 6-15 glutathione-disulfide reductase Homo sapiens 111-132 29928421-10 2018 The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P<0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P<0.05). celastrol 62-72 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 32-37 29928421-10 2018 The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P<0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P<0.05). celastrol 62-72 caspase 3 Homo sapiens 162-171 29928421-10 2018 The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P<0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P<0.05). celastrol 62-72 BCL2 associated X, apoptosis regulator Homo sapiens 176-179 29928421-11 2018 The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax. celastrol 32-42 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 205-210 29928421-11 2018 The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax. celastrol 32-42 caspase 3 Homo sapiens 247-256 29928421-11 2018 The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax. celastrol 32-42 BCL2 associated X, apoptosis regulator Homo sapiens 261-264 29493374-4 2018 OBJECTIVE: This study investigated the effect of celastrol on mRNA expression and concentration levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL6) that are induced by influenza A/Puerto Rico/8/34 (H1N1; PR8) in Madin-Darby Canine Kidney (MDCK) cells. celastrol 49-58 interleukin 6 Homo sapiens 195-198 29493374-9 2018 RESULTS: mRNA expression and concentrations of TNFalpha and IL6 increased significantly in control virus compared to cell control, and decreased significantly when compared with control virus after celastrol treatment. celastrol 198-207 tumor necrosis factor Homo sapiens 47-55 29493374-9 2018 RESULTS: mRNA expression and concentrations of TNFalpha and IL6 increased significantly in control virus compared to cell control, and decreased significantly when compared with control virus after celastrol treatment. celastrol 198-207 interleukin 6 Homo sapiens 60-63 29493374-11 2018 CONCLUSION: Due to reducing mRNA expression and concentrations of TNFalpha and IL6, celastrol can serve as a suitable choice to control cytokine-induced inflammation in IAV infection, and therefore it can be used with current antiviral drugs. celastrol 84-93 tumor necrosis factor Homo sapiens 66-74 29493374-11 2018 CONCLUSION: Due to reducing mRNA expression and concentrations of TNFalpha and IL6, celastrol can serve as a suitable choice to control cytokine-induced inflammation in IAV infection, and therefore it can be used with current antiviral drugs. celastrol 84-93 interleukin 6 Homo sapiens 79-82 29274099-0 2018 Effects of celastrol on Tau hyperphosphorylation and expression of HSF-1 and HSP70 in SH-SY5Y neuroblastoma cells induced by amyloid-beta peptides. celastrol 11-20 heat shock transcription factor 1 Homo sapiens 67-72 29789558-0 2018 Celastrol alleviates renal fibrosis by upregulating cannabinoid receptor 2 expression. celastrol 0-9 cannabinoid receptor 2 (macrophage) Mus musculus 52-74 29789558-7 2018 Furthermore, celastrol potentiated the expression of the anti-fibrotic factor cannabinoid receptor 2 (CB2R) in established mouse fibrotic kidney tissues and transforming growth factor beta1 (TGF-beta1)-stimulated human kidney 2 (HK-2) cells. celastrol 13-22 cannabinoid receptor 2 (macrophage) Mus musculus 78-100 29789558-7 2018 Furthermore, celastrol potentiated the expression of the anti-fibrotic factor cannabinoid receptor 2 (CB2R) in established mouse fibrotic kidney tissues and transforming growth factor beta1 (TGF-beta1)-stimulated human kidney 2 (HK-2) cells. celastrol 13-22 cannabinoid receptor 2 (macrophage) Mus musculus 102-106 29789558-8 2018 In addition, the CB2R antagonist (SR144528) abolished celastrol-mediated beneficial effects on renal fibrosis. celastrol 54-63 cannabinoid receptor 2 (macrophage) Mus musculus 17-21 29789558-9 2018 Moreover, UUO- or TGF-beta1-induced activation of the pro-fibrotic factor SMAD family member 3 (Smad3) was markedly inhibited by celastrol. celastrol 129-138 transforming growth factor, beta 1 Mus musculus 18-27 29789558-9 2018 Moreover, UUO- or TGF-beta1-induced activation of the pro-fibrotic factor SMAD family member 3 (Smad3) was markedly inhibited by celastrol. celastrol 129-138 SMAD family member 3 Mus musculus 96-101 29789558-11 2018 In conclusion, our study provides the first direct evidence that celastrol significantly alleviated renal fibrosis, by contributing to the upregulation of CB2R expression through inhibiting Smad3 signaling pathway activation. celastrol 65-74 cannabinoid receptor 2 (macrophage) Mus musculus 155-159 29789558-11 2018 In conclusion, our study provides the first direct evidence that celastrol significantly alleviated renal fibrosis, by contributing to the upregulation of CB2R expression through inhibiting Smad3 signaling pathway activation. celastrol 65-74 SMAD family member 3 Mus musculus 190-195 29274099-0 2018 Effects of celastrol on Tau hyperphosphorylation and expression of HSF-1 and HSP70 in SH-SY5Y neuroblastoma cells induced by amyloid-beta peptides. celastrol 11-20 heat shock protein family A (Hsp70) member 4 Homo sapiens 77-82 29274099-5 2018 Meanwhile, both celastrol treatment and knockdown of HSP70 or HSF-1 in SH-SY5Y cells significantly inhibited the Tau hyperphosphorylation and HSP90 expression induced by Abeta1-42 . celastrol 16-25 heat shock protein 90 alpha family class A member 1 Homo sapiens 142-147 29484434-0 2018 miR-33a-5p enhances the sensitivity of lung adenocarcinoma cells to celastrol by regulating mTOR signaling. celastrol 68-77 MLX interacting protein Homo sapiens 0-3 29484434-13 2018 In summary, miR-33a-5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo. celastrol 153-162 mechanistic target of rapamycin kinase Homo sapiens 176-180 29765532-4 2018 With the use of flow cytometry we have shown that celastrol reduces the cell size of the SP (side population; subpopulation of cancer cells enriched with cancer stem cells), increases frequency of apoptosis and binds to Pgp protein in cell membranes inhibiting its transport function. celastrol 50-59 phosphoglycolate phosphatase Homo sapiens 220-223 29484434-0 2018 miR-33a-5p enhances the sensitivity of lung adenocarcinoma cells to celastrol by regulating mTOR signaling. celastrol 68-77 mechanistic target of rapamycin kinase Homo sapiens 92-96 29484434-6 2018 Following treatment with celastrol, miR-33a-5p expression was upregulated, and miR-33a-5p could enhance cellular sensitivity to celastrol. celastrol 25-34 MLX interacting protein Homo sapiens 36-39 29484434-6 2018 Following treatment with celastrol, miR-33a-5p expression was upregulated, and miR-33a-5p could enhance cellular sensitivity to celastrol. celastrol 25-34 MLX interacting protein Homo sapiens 79-82 29484434-6 2018 Following treatment with celastrol, miR-33a-5p expression was upregulated, and miR-33a-5p could enhance cellular sensitivity to celastrol. celastrol 128-137 MLX interacting protein Homo sapiens 79-82 29484434-7 2018 Western blot analysis revealed that the expression of mTOR, p-p70S6K and p-4EBP1 decreased following celastrol treatment. celastrol 101-110 mechanistic target of rapamycin kinase Homo sapiens 54-58 29484434-7 2018 Western blot analysis revealed that the expression of mTOR, p-p70S6K and p-4EBP1 decreased following celastrol treatment. celastrol 101-110 ribosomal protein S6 kinase B1 Homo sapiens 62-68 29484434-7 2018 Western blot analysis revealed that the expression of mTOR, p-p70S6K and p-4EBP1 decreased following celastrol treatment. celastrol 101-110 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 75-80 29484434-8 2018 These results suggested that mTOR was involved in the mechanism by which miR-33a-5p enhanced the sensitivity of lung adenocarcinoma cells to celastrol. celastrol 141-150 mechanistic target of rapamycin kinase Homo sapiens 29-33 29484434-8 2018 These results suggested that mTOR was involved in the mechanism by which miR-33a-5p enhanced the sensitivity of lung adenocarcinoma cells to celastrol. celastrol 141-150 MLX interacting protein Homo sapiens 73-76 29484434-12 2018 In addition, celastrol upregulated the expression of miR-33a-5p, and high expression of miR-33a-5p inhibited mTOR and its downstream effectors. celastrol 13-22 MLX interacting protein Homo sapiens 53-56 29484434-12 2018 In addition, celastrol upregulated the expression of miR-33a-5p, and high expression of miR-33a-5p inhibited mTOR and its downstream effectors. celastrol 13-22 MLX interacting protein Homo sapiens 88-91 29484434-12 2018 In addition, celastrol upregulated the expression of miR-33a-5p, and high expression of miR-33a-5p inhibited mTOR and its downstream effectors. celastrol 13-22 mechanistic target of rapamycin kinase Homo sapiens 109-113 29484434-13 2018 In summary, miR-33a-5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo. celastrol 114-123 MLX interacting protein Homo sapiens 12-15 29484434-13 2018 In summary, miR-33a-5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo. celastrol 153-162 MLX interacting protein Homo sapiens 12-15 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 hexokinase 2 Rattus norvegicus 97-100 29534015-2 2018 Here, we report the antitumor effect of celastrol, an anti-inflammatory compound and a recognized HSP90 inhibitor, in Hodgkin and Reed-Sternberg cell lines. celastrol 40-49 heat shock protein 90 alpha family class A member 1 Homo sapiens 98-103 29534015-4 2018 In KM-H2 cells, celastrol inhibited cell proliferation, induced G0/G1 arrest, and triggered apoptosis through the activation of caspase-3/7. celastrol 16-25 caspase 3 Homo sapiens 128-137 29534015-6 2018 A proteomic screening identified a total of 262 differentially expressed proteins in sensitive KM-H2 cells and revealed that celastrol"s toxicity involved the suppression of the MAPK/ERK (extracellular signal regulated kinase/mitogen activated protein kinase) pathway. celastrol 125-134 mitogen-activated protein kinase 3 Homo sapiens 178-182 29534015-6 2018 A proteomic screening identified a total of 262 differentially expressed proteins in sensitive KM-H2 cells and revealed that celastrol"s toxicity involved the suppression of the MAPK/ERK (extracellular signal regulated kinase/mitogen activated protein kinase) pathway. celastrol 125-134 mitogen-activated protein kinase 3 Homo sapiens 183-186 29534015-8 2018 The L428 resistant cells exhibited a marked induction of HSP27 mRNA and protein after celastrol treatment. celastrol 86-95 heat shock protein family B (small) member 1 Homo sapiens 57-62 29534015-9 2018 Our results provide the first evidence that celastrol has antitumor effects in cHL cells through the suppression of the MAPK/ERK pathway. celastrol 44-53 mitogen-activated protein kinase 3 Homo sapiens 120-124 29534015-9 2018 Our results provide the first evidence that celastrol has antitumor effects in cHL cells through the suppression of the MAPK/ERK pathway. celastrol 44-53 mitogen-activated protein kinase 3 Homo sapiens 125-128 29534015-10 2018 Resistance to celastrol has rarely been described, and our results suggest that in cHL it may be mediated by the upregulation of HSP27. celastrol 14-23 heat shock protein family B (small) member 1 Homo sapiens 129-134 29540209-0 2018 Celastrol treatment protects against acute ischemic stroke-induced brain injury by promoting an IL-33/ST2 axis-mediated microglia/macrophage M2 polarization. celastrol 0-9 interleukin 33 Homo sapiens 96-101 29540209-0 2018 Celastrol treatment protects against acute ischemic stroke-induced brain injury by promoting an IL-33/ST2 axis-mediated microglia/macrophage M2 polarization. celastrol 0-9 ST2 Homo sapiens 102-105 29540209-7 2018 Furthermore, in vitro experiments confirmed that celastrol treatment decreased inflammatory cytokine expression induced by OGD through an IL-33/ST2 axis-mediated M2 microglia/macrophage polarization. celastrol 49-58 interleukin 33 Homo sapiens 138-143 29540209-7 2018 Furthermore, in vitro experiments confirmed that celastrol treatment decreased inflammatory cytokine expression induced by OGD through an IL-33/ST2 axis-mediated M2 microglia/macrophage polarization. celastrol 49-58 ST2 Homo sapiens 144-147 29475002-0 2018 Celastrol pretreatment attenuates rat myocardial ischemia/ reperfusion injury by inhibiting high mobility group box 1 protein expression via the PI3K/Akt pathway. celastrol 0-9 high mobility group box 1 Rattus norvegicus 92-117 29475002-0 2018 Celastrol pretreatment attenuates rat myocardial ischemia/ reperfusion injury by inhibiting high mobility group box 1 protein expression via the PI3K/Akt pathway. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 150-153 29475002-2 2018 This study aimed to investigate the cardioprotective effects of celastrol pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the phosphoinositide 3-kinase (PI3K)/Akt pathway. celastrol 64-73 high mobility group box 1 Rattus norvegicus 229-234 29475002-2 2018 This study aimed to investigate the cardioprotective effects of celastrol pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the phosphoinositide 3-kinase (PI3K)/Akt pathway. celastrol 64-73 AKT serine/threonine kinase 1 Rattus norvegicus 288-291 29475002-7 2018 Additionally, celastrol downregulated HMGB1 expression and upregulated p-Akt expression in the myocardium. celastrol 14-23 high mobility group box 1 Rattus norvegicus 38-43 29475002-7 2018 Additionally, celastrol downregulated HMGB1 expression and upregulated p-Akt expression in the myocardium. celastrol 14-23 AKT serine/threonine kinase 1 Rattus norvegicus 73-76 29475002-8 2018 LY294002, a specific pI3k inhibitor, partially reversed the decreased HMGB1 expression, increased p-Akt expression induced by celastrol, and abolished the anti-apoptotic, anti-inflammatory and anti-oxidative effects of celastrol. celastrol 126-135 AKT serine/threonine kinase 1 Rattus norvegicus 100-103 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 mechanistic target of rapamycin kinase Rattus norvegicus 117-121 29475002-9 2018 CONCLUSION: These findings suggest that short-term pretreatment with celastrol protects against myocardial I/R injury by suppressing myocardial apoptosis, inflammatory response and oxidative stress via pI3k/Akt pathway activation and HMGB1 inhibition. celastrol 69-78 AKT serine/threonine kinase 1 Rattus norvegicus 207-210 29475002-9 2018 CONCLUSION: These findings suggest that short-term pretreatment with celastrol protects against myocardial I/R injury by suppressing myocardial apoptosis, inflammatory response and oxidative stress via pI3k/Akt pathway activation and HMGB1 inhibition. celastrol 69-78 high mobility group box 1 Rattus norvegicus 234-239 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 123-133 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 135-140 29476742-2 2018 Celastrol, a Chinese herbal compound that has anti-inflammatory and immunosuppressive properties, has been indicated to suppress T cell proliferation and Th17 cell induction, while facilitating Forkhead box P3 (Foxp3) expression and Treg cell generation. celastrol 0-9 forkhead box P3 Rattus norvegicus 194-209 29476742-2 2018 Celastrol, a Chinese herbal compound that has anti-inflammatory and immunosuppressive properties, has been indicated to suppress T cell proliferation and Th17 cell induction, while facilitating Forkhead box P3 (Foxp3) expression and Treg cell generation. celastrol 0-9 forkhead box P3 Rattus norvegicus 211-216 29476742-5 2018 Initially, we determined that Interleukin (IL)-17 expression by celastrol-treated Th17 was significantly decreased compared with untreated cells; however, the frequency of Foxp3+ cells was increased in celastrol-treated cells. celastrol 64-73 interleukin 17A Rattus norvegicus 30-49 29476742-5 2018 Initially, we determined that Interleukin (IL)-17 expression by celastrol-treated Th17 was significantly decreased compared with untreated cells; however, the frequency of Foxp3+ cells was increased in celastrol-treated cells. celastrol 202-211 forkhead box P3 Rattus norvegicus 172-177 29476742-6 2018 We verified that celastrol inhibited phospho-STAT3 expression in cultured Th17 cells and up-regulated phospho-STAT5 expression in iTreg cells. celastrol 17-26 signal transducer and activator of transcription 3 Rattus norvegicus 45-50 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 145-148 29476742-9 2018 Conversely, celastrol promoted FAO of lipids by up-regulating CPT1A and AMPKalpha expression in iTreg cells. celastrol 12-21 carnitine palmitoyltransferase 1A Rattus norvegicus 62-67 29476742-6 2018 We verified that celastrol inhibited phospho-STAT3 expression in cultured Th17 cells and up-regulated phospho-STAT5 expression in iTreg cells. celastrol 17-26 signal transducer and activator of transcription 5A Rattus norvegicus 110-115 29476742-8 2018 Celastrol suppressed the expression of glucose transporter, Glut1, and the rate-limiting enzyme, HK2, in addition to mTOR, HIF-1alpha, c-Myc and Akt expression in Th17 cells. celastrol 0-9 solute carrier family 2 member 1 Rattus norvegicus 60-65 30250883-2 2018 We recently identified a critical role of nuclear receptor Nur77 and celastrol in priming inflamed mitochondria for autophagy through its mitochondrial targeting and interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2) and the autophagic adaptor p62/SQSTM1. celastrol 69-78 TNF receptor associated factor 2 Homo sapiens 183-233 30250883-2 2018 We recently identified a critical role of nuclear receptor Nur77 and celastrol in priming inflamed mitochondria for autophagy through its mitochondrial targeting and interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2) and the autophagic adaptor p62/SQSTM1. celastrol 69-78 TNF receptor associated factor 2 Homo sapiens 235-240 30250883-2 2018 We recently identified a critical role of nuclear receptor Nur77 and celastrol in priming inflamed mitochondria for autophagy through its mitochondrial targeting and interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2) and the autophagic adaptor p62/SQSTM1. celastrol 69-78 sequestosome 1 Homo sapiens 269-272 30250883-2 2018 We recently identified a critical role of nuclear receptor Nur77 and celastrol in priming inflamed mitochondria for autophagy through its mitochondrial targeting and interaction with tumor necrosis factor receptor-associated factor 2 (TRAF2) and the autophagic adaptor p62/SQSTM1. celastrol 69-78 sequestosome 1 Homo sapiens 273-279 29090408-5 2018 Small interfering RNA (siRNA) knockdown of HSPA6 and HSPA1A resulted in loss of the protective effect of co-application of celastrol/arimoclomol. celastrol 123-132 heat shock protein family A (Hsp70) member 6 Homo sapiens 43-48 28726161-0 2018 Celastrol specifically inhibits the activation of NLRP3 inflammasome. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 50-55 29394256-0 2018 The natural anti-tumor compound Celastrol targets a Myb-C/EBPbeta-p300 transcriptional module implicated in myeloid gene expression. celastrol 32-41 myeloblastosis oncogene Mus musculus 52-55 29394256-0 2018 The natural anti-tumor compound Celastrol targets a Myb-C/EBPbeta-p300 transcriptional module implicated in myeloid gene expression. celastrol 32-41 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 56-65 29394256-0 2018 The natural anti-tumor compound Celastrol targets a Myb-C/EBPbeta-p300 transcriptional module implicated in myeloid gene expression. celastrol 32-41 E1A binding protein p300 Mus musculus 66-70 29394256-2 2018 Using a myeloid cell line with a stably integrated Myb-inducible reporter gene as a screening tool we have previously identified Celastrol, a natural compound with anti-tumor activity, as a potent Myb inhibitor that disrupts the interaction of Myb with the co-activator p300. celastrol 129-138 myeloblastosis oncogene Mus musculus 51-54 29394256-2 2018 Using a myeloid cell line with a stably integrated Myb-inducible reporter gene as a screening tool we have previously identified Celastrol, a natural compound with anti-tumor activity, as a potent Myb inhibitor that disrupts the interaction of Myb with the co-activator p300. celastrol 129-138 myeloblastosis oncogene Mus musculus 197-200 29394256-2 2018 Using a myeloid cell line with a stably integrated Myb-inducible reporter gene as a screening tool we have previously identified Celastrol, a natural compound with anti-tumor activity, as a potent Myb inhibitor that disrupts the interaction of Myb with the co-activator p300. celastrol 129-138 myeloblastosis oncogene Mus musculus 197-200 29394256-2 2018 Using a myeloid cell line with a stably integrated Myb-inducible reporter gene as a screening tool we have previously identified Celastrol, a natural compound with anti-tumor activity, as a potent Myb inhibitor that disrupts the interaction of Myb with the co-activator p300. celastrol 129-138 E1A binding protein p300 Mus musculus 270-274 29394256-3 2018 We showed that Celastrol inhibits the proliferation of acute myeloid leukemia (AML) cells and prolongs the survival of mice in an in vivo model of AML, demonstrating that targeting Myb with a small-molecule inhibitor is feasible and might have potential as a therapeutic approach against AML. celastrol 15-24 myeloblastosis oncogene Mus musculus 181-184 29394256-5 2018 By re-investigating the inhibitory potential of Celastrol we have found that Celastrol also strongly inhibits the activity of C/EBPbeta by disrupting its interaction with the Taz2 domain of p300. celastrol 48-57 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 126-135 29394256-5 2018 By re-investigating the inhibitory potential of Celastrol we have found that Celastrol also strongly inhibits the activity of C/EBPbeta by disrupting its interaction with the Taz2 domain of p300. celastrol 48-57 E1A binding protein p300 Mus musculus 190-194 29394256-5 2018 By re-investigating the inhibitory potential of Celastrol we have found that Celastrol also strongly inhibits the activity of C/EBPbeta by disrupting its interaction with the Taz2 domain of p300. celastrol 77-86 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 126-135 29394256-5 2018 By re-investigating the inhibitory potential of Celastrol we have found that Celastrol also strongly inhibits the activity of C/EBPbeta by disrupting its interaction with the Taz2 domain of p300. celastrol 77-86 E1A binding protein p300 Mus musculus 190-194 29394256-6 2018 Together with previous studies our work reveals that Celastrol independently targets Myb and C/EBPbeta by disrupting the interaction of both transcription factors with p300. celastrol 53-62 myeloblastosis oncogene Mus musculus 85-88 29394256-6 2018 Together with previous studies our work reveals that Celastrol independently targets Myb and C/EBPbeta by disrupting the interaction of both transcription factors with p300. celastrol 53-62 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 93-102 29394256-6 2018 Together with previous studies our work reveals that Celastrol independently targets Myb and C/EBPbeta by disrupting the interaction of both transcription factors with p300. celastrol 53-62 E1A binding protein p300 Mus musculus 168-172 29394256-8 2018 We hypothesize that the ability of Celastrol to disrupt the activity of a transcriptional Myb-C/EBPbeta-p300 module might explain its promising anti-leukemic activity. celastrol 35-44 myeloblastosis oncogene Mus musculus 90-93 29394256-8 2018 We hypothesize that the ability of Celastrol to disrupt the activity of a transcriptional Myb-C/EBPbeta-p300 module might explain its promising anti-leukemic activity. celastrol 35-44 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 94-103 29394256-8 2018 We hypothesize that the ability of Celastrol to disrupt the activity of a transcriptional Myb-C/EBPbeta-p300 module might explain its promising anti-leukemic activity. celastrol 35-44 E1A binding protein p300 Mus musculus 104-108 29090408-5 2018 Small interfering RNA (siRNA) knockdown of HSPA6 and HSPA1A resulted in loss of the protective effect of co-application of celastrol/arimoclomol. celastrol 123-132 heat shock protein family A (Hsp70) member 1A Homo sapiens 53-59 30068874-6 2018 Western blot analysis revealed that expression of indoleamine 2,3-dioxygenase (IDO), the enzyme catalyzing Trp to generate Kyn, was dramatically inhibited in colon cancer cells after celastrol treatment, with a dose-dependent manner. celastrol 183-192 indoleamine 2,3-dioxygenase 1 Homo sapiens 50-77 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 signal transducer and activator of transcription 3 Homo sapiens 58-108 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 signal transducer and activator of transcription 3 Homo sapiens 110-115 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 125-142 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 144-149 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 151-156 29434967-6 2018 Celastrol may also decrease the phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and the B cell lymphoma-2 (Bcl-2)/Bcl-2 associated C protein (Bax) ratio. celastrol 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 179-182 29445341-2 2018 Numerous studies have shown that Interleukin (IL)-17 producing CD4+T cells (Th17 cells), which could be inhibited by celastrol, is essential in mediating steroid-resistant AHR. celastrol 117-126 interleukin 17A Mus musculus 33-52 29445341-12 2018 Moreover, celastrol treatment decreased the frequency of Th17 cell expansion and reduced the production of IL-17A in both lung and serum. celastrol 10-19 interleukin 17A Mus musculus 107-113 29069290-3 2018 Dietary celastrol (31.25 ppm in rodent diet from 8 weeks to 25 weeks of age) is well tolerated and protects against LPS-induced acute inflammation in C57BL/6 mice, potently suppressing LPS-induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, Interleukin (IL)-6 and IL-1beta. celastrol 8-17 nitric oxide synthase 2, inducible Mus musculus 202-233 29069290-3 2018 Dietary celastrol (31.25 ppm in rodent diet from 8 weeks to 25 weeks of age) is well tolerated and protects against LPS-induced acute inflammation in C57BL/6 mice, potently suppressing LPS-induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, Interleukin (IL)-6 and IL-1beta. celastrol 8-17 nitric oxide synthase 2, inducible Mus musculus 235-239 29069290-3 2018 Dietary celastrol (31.25 ppm in rodent diet from 8 weeks to 25 weeks of age) is well tolerated and protects against LPS-induced acute inflammation in C57BL/6 mice, potently suppressing LPS-induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, Interleukin (IL)-6 and IL-1beta. celastrol 8-17 cytochrome c oxidase II, mitochondrial Mus musculus 242-264 29069290-3 2018 Dietary celastrol (31.25 ppm in rodent diet from 8 weeks to 25 weeks of age) is well tolerated and protects against LPS-induced acute inflammation in C57BL/6 mice, potently suppressing LPS-induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, Interleukin (IL)-6 and IL-1beta. celastrol 8-17 interleukin 6 Mus musculus 266-284 29069290-3 2018 Dietary celastrol (31.25 ppm in rodent diet from 8 weeks to 25 weeks of age) is well tolerated and protects against LPS-induced acute inflammation in C57BL/6 mice, potently suppressing LPS-induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, Interleukin (IL)-6 and IL-1beta. celastrol 8-17 interleukin 1 beta Mus musculus 289-297 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 122-126 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 151-155 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 cytochrome c oxidase II, mitochondrial Mus musculus 157-162 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 167-175 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 interleukin 6 Mus musculus 250-254 29069290-6 2018 Celastrol chemoprevention of CAC in this new model of intestinal neoplasia was associated with significant suppression of iNOS at 4 months of age, and iNOS, COX-2 and NFkappaB at 6 months of age, with significant reduction in inflammatory cytokines, IL-6 and IL-1beta. celastrol 0-9 interleukin 1 beta Mus musculus 259-267 30068874-6 2018 Western blot analysis revealed that expression of indoleamine 2,3-dioxygenase (IDO), the enzyme catalyzing Trp to generate Kyn, was dramatically inhibited in colon cancer cells after celastrol treatment, with a dose-dependent manner. celastrol 183-192 indoleamine 2,3-dioxygenase 1 Homo sapiens 79-82 30068874-7 2018 These results suggest that suppression of IDO expression and tryptophan catabolism may be part of the mechanisms of celastrol in its cytotoxic effect against HCT116 colon cancer cells. celastrol 116-125 indoleamine 2,3-dioxygenase 1 Homo sapiens 42-45 28994112-0 2018 Celastrol attenuates pain and cartilage damage via SDF-1/CXCR4 signalling pathway in osteoarthritis rats. celastrol 0-9 C-X-C motif chemokine receptor 4 Rattus norvegicus 57-62 28994112-1 2018 OBJECTIVES: Celastrol has attracted wide interests for its anticancer and anti-inflammation properties, and studies have demonstrated that celastrol negatively modulates the stromal cell-derived factor-1 (SDF-1) and receptor C-X-C chemokine receptor type 4 (CXCR4) signalling. celastrol 139-148 C-X-C motif chemokine ligand 12 Rattus norvegicus 174-203 28994112-1 2018 OBJECTIVES: Celastrol has attracted wide interests for its anticancer and anti-inflammation properties, and studies have demonstrated that celastrol negatively modulates the stromal cell-derived factor-1 (SDF-1) and receptor C-X-C chemokine receptor type 4 (CXCR4) signalling. celastrol 139-148 C-X-C motif chemokine ligand 12 Rattus norvegicus 205-210 28994112-1 2018 OBJECTIVES: Celastrol has attracted wide interests for its anticancer and anti-inflammation properties, and studies have demonstrated that celastrol negatively modulates the stromal cell-derived factor-1 (SDF-1) and receptor C-X-C chemokine receptor type 4 (CXCR4) signalling. celastrol 139-148 C-X-C motif chemokine receptor 4 Rattus norvegicus 225-256 28994112-1 2018 OBJECTIVES: Celastrol has attracted wide interests for its anticancer and anti-inflammation properties, and studies have demonstrated that celastrol negatively modulates the stromal cell-derived factor-1 (SDF-1) and receptor C-X-C chemokine receptor type 4 (CXCR4) signalling. celastrol 139-148 C-X-C motif chemokine receptor 4 Rattus norvegicus 258-263 28994112-5 2018 KEY FINDINGS: Celastrol significantly attenuated the joint pain and cartilage damage induced by MIA in OA rats and suppressed the upregulation of SDF-1/CXCR4 and associated genes caused by MIA injections. celastrol 14-23 C-X-C motif chemokine ligand 12 Rattus norvegicus 146-151 28994112-5 2018 KEY FINDINGS: Celastrol significantly attenuated the joint pain and cartilage damage induced by MIA in OA rats and suppressed the upregulation of SDF-1/CXCR4 and associated genes caused by MIA injections. celastrol 14-23 C-X-C motif chemokine receptor 4 Rattus norvegicus 152-157 28994112-7 2018 CONCLUSIONS: Celastrol ameliorate OA in vivo as evidenced by the attenuated joint pain and less cartilage damage in OA rats given celastrol treatments, an effect mediated via suppression of the SDF-1/CXCR4 pathway. celastrol 13-22 C-X-C motif chemokine ligand 12 Rattus norvegicus 194-199 28994112-7 2018 CONCLUSIONS: Celastrol ameliorate OA in vivo as evidenced by the attenuated joint pain and less cartilage damage in OA rats given celastrol treatments, an effect mediated via suppression of the SDF-1/CXCR4 pathway. celastrol 13-22 C-X-C motif chemokine receptor 4 Rattus norvegicus 200-205 28994112-7 2018 CONCLUSIONS: Celastrol ameliorate OA in vivo as evidenced by the attenuated joint pain and less cartilage damage in OA rats given celastrol treatments, an effect mediated via suppression of the SDF-1/CXCR4 pathway. celastrol 130-139 C-X-C motif chemokine ligand 12 Rattus norvegicus 194-199 28994112-7 2018 CONCLUSIONS: Celastrol ameliorate OA in vivo as evidenced by the attenuated joint pain and less cartilage damage in OA rats given celastrol treatments, an effect mediated via suppression of the SDF-1/CXCR4 pathway. celastrol 130-139 C-X-C motif chemokine receptor 4 Rattus norvegicus 200-205 29256892-10 2017 Moreover, treatment with 50 nM celastrol significantly downregulated mRNA and protein expression of TNF-alpha and IL-1ss. celastrol 31-40 tumor necrosis factor Rattus norvegicus 100-109 29902110-0 2018 Celastrol enhances Atoh1 expression in inner ear stem cells and promotes their differentiation into functional auditory neuronal-like cells. celastrol 0-9 atonal bHLH transcription factor 1 Mus musculus 19-24 29902110-11 2018 Most notably, these effects were apparently associated with the upregulation of Atoh1 in response to Celastrol treatment. celastrol 101-110 atonal bHLH transcription factor 1 Mus musculus 80-85 29270590-9 2017 Pharmacological inhibitors of MEK (PD98059, 10 mumol/L) or Akt (MK2206, 10 mumol/L) could reverse the phosphorylation of ERK1/2 and Akt, and abolish up-regulation of GCLC and GST induced by celastrol at mRNA levels. celastrol 190-199 midkine Mus musculus 30-33 29270590-9 2017 Pharmacological inhibitors of MEK (PD98059, 10 mumol/L) or Akt (MK2206, 10 mumol/L) could reverse the phosphorylation of ERK1/2 and Akt, and abolish up-regulation of GCLC and GST induced by celastrol at mRNA levels. celastrol 190-199 thymoma viral proto-oncogene 1 Mus musculus 59-62 29270590-9 2017 Pharmacological inhibitors of MEK (PD98059, 10 mumol/L) or Akt (MK2206, 10 mumol/L) could reverse the phosphorylation of ERK1/2 and Akt, and abolish up-regulation of GCLC and GST induced by celastrol at mRNA levels. celastrol 190-199 mitogen-activated protein kinase 3 Mus musculus 121-127 29270590-10 2017 Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1G93ANSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation. celastrol 33-42 superoxide dismutase 1, soluble Mus musculus 85-89 29270590-10 2017 Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1G93ANSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation. celastrol 33-42 midkine Mus musculus 134-137 29270590-10 2017 Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1G93ANSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation. celastrol 33-42 mitogen-activated protein kinase 1 Mus musculus 138-141 29270590-10 2017 Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1G93ANSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation. celastrol 33-42 thymoma viral proto-oncogene 1 Mus musculus 151-154 29270590-2 2017 SOD1G93A transfected NSC34 cells were treated with different doses of H2O2 and celastrol. celastrol 79-88 superoxide dismutase 1, soluble Mus musculus 0-4 29270590-6 2017 The results showed that pre-incubation of celastrol (50 nmol/L) for 4 h prior to H2O2 (10 mumol/L) co-treatment for another 24 h significantly attenuated H2O2-induced cell death and MDA level in SOD1G93A transfected NSC34 cells. celastrol 42-51 superoxide dismutase 1, soluble Mus musculus 195-199 29270590-7 2017 Real-time PCR showed that the mRNA expressions of GCLC and GST were enhanced with pre-incubation of celastrol. celastrol 100-109 glutamate-cysteine ligase, catalytic subunit Mus musculus 50-54 29270590-8 2017 Celastrol quickly induced phosphorylation of ERK1/2 and Akt within 30 min and 1 h respectively in SOD1G93A transfected NSC34 cells. celastrol 0-9 mitogen-activated protein kinase 3 Mus musculus 45-51 29270590-8 2017 Celastrol quickly induced phosphorylation of ERK1/2 and Akt within 30 min and 1 h respectively in SOD1G93A transfected NSC34 cells. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 56-59 29270590-8 2017 Celastrol quickly induced phosphorylation of ERK1/2 and Akt within 30 min and 1 h respectively in SOD1G93A transfected NSC34 cells. celastrol 0-9 superoxide dismutase 1, soluble Mus musculus 98-102 29202812-0 2017 Celastrol improves self-renewal and differentiation of human tendon-derived stem cells by suppressing Smad7 through hypoxia. celastrol 0-9 SMAD family member 7 Homo sapiens 102-107 29202812-9 2017 Celastrol elicited hypoxia and subsequently suppressed the expression of Smad7 through direct association with the hypoxia response element consensus sequence. celastrol 0-9 SMAD family member 7 Homo sapiens 73-78 29202812-10 2017 Further, we demonstrated that both Smad7 and HIF1alpha were involved in the beneficial effects of celastrol on the differentiation and self-renewal of hTSCs. celastrol 98-107 SMAD family member 7 Homo sapiens 35-40 29202812-10 2017 Further, we demonstrated that both Smad7 and HIF1alpha were involved in the beneficial effects of celastrol on the differentiation and self-renewal of hTSCs. celastrol 98-107 hypoxia inducible factor 1 subunit alpha Homo sapiens 45-54 29256892-12 2017 CONCLUSION: Our study demonstrated that low-dose celastrol could prevent MIRI in cardiomyocytes by inhibiting the activation of NF-K B, and celastrol may be a potential therapeutic agent for preventing MIRI. celastrol 49-58 nuclear factor kappa B subunit 1 Rattus norvegicus 128-134 28944849-0 2017 Celastrol alleviates angiotensin II-mediated vascular smooth muscle cell senescence via induction of autophagy. celastrol 0-9 angiotensinogen Homo sapiens 21-35 29048668-0 2017 Celastrol downregulates E2F1 to induce growth inhibitory effects in hepatocellular carcinoma HepG2 cells. celastrol 0-9 E2F transcription factor 1 Homo sapiens 24-28 29048668-5 2017 E2F1 was potently downregulated by celastrol in a dose- and time-dependent manner at both the mRNA and protein levels. celastrol 35-44 E2F transcription factor 1 Homo sapiens 0-4 29048668-6 2017 Moreover, siRNA-mediated E2F1 silencing enhanced celastrol-induced apoptosis and inhibition of proliferation. celastrol 49-58 E2F transcription factor 1 Homo sapiens 25-29 29048668-7 2017 Our data imply that downregulation of E2F1 may be a key factor in the celastrol-mediated inhibitory effects in HepG2 cells, and celastrol can serve as a leading compound for the development of compounds designed to inactivate E2F1 for HCC therapy. celastrol 70-79 E2F transcription factor 1 Homo sapiens 38-42 29048668-7 2017 Our data imply that downregulation of E2F1 may be a key factor in the celastrol-mediated inhibitory effects in HepG2 cells, and celastrol can serve as a leading compound for the development of compounds designed to inactivate E2F1 for HCC therapy. celastrol 70-79 E2F transcription factor 1 Homo sapiens 226-230 27931154-0 2017 Inhibition of IKKbeta by celastrol and its analogues - an in silico and in vitro approach. celastrol 25-34 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 14-21 27931154-4 2017 OBJECTIVE: This study determines the neuroprotective and inhibitory effect of celastrol on amyloid beta1-42 (Abeta1-42) induced cytotoxicity and IKKbeta activity, respectively. celastrol 78-87 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 145-152 27931154-6 2017 We screened 36 celastrol analogues for the IKKbeta inhibition by molecular docking and evaluated their drug like properties to delineate the neuroprotective effects. celastrol 15-24 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 43-50 27931154-7 2017 RESULTS: Celastrol (1 muM) inhibited Abeta1-42 (10 muM) induced IkappaBalpha phosphorylation and protected IMR-32 cells from cell death. celastrol 9-18 NFKB inhibitor alpha Homo sapiens 64-76 27931154-8 2017 Celastrol and 25 analogues showed strong binding affinity with IKKbeta as evidenced by strong hydrogen-bonding interactions with critical active site residues. celastrol 0-9 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 63-70 27931154-12 2017 The neuroprotective potentials of celastrol and its analogues may be related to IKK inhibition. celastrol 34-43 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 80-83 29040966-0 2017 Natural product celastrol suppressed macrophage M1 polarization against inflammation in diet-induced obese mice via regulating Nrf2/HO-1, MAP kinase and NF-kappaB pathways. celastrol 16-25 nuclear factor, erythroid derived 2, like 2 Mus musculus 127-131 29040966-0 2017 Natural product celastrol suppressed macrophage M1 polarization against inflammation in diet-induced obese mice via regulating Nrf2/HO-1, MAP kinase and NF-kappaB pathways. celastrol 16-25 heme oxygenase 1 Mus musculus 132-136 29040966-5 2017 Celastrol down-regulated the mRNA levels of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in cell culture and in mice. celastrol 0-9 interleukin 6 Mus musculus 76-80 29040966-5 2017 Celastrol down-regulated the mRNA levels of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in cell culture and in mice. celastrol 0-9 interleukin 1 beta Mus musculus 82-90 29040966-5 2017 Celastrol down-regulated the mRNA levels of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in cell culture and in mice. celastrol 0-9 tumor necrosis factor Mus musculus 92-101 29040966-5 2017 Celastrol down-regulated the mRNA levels of macrophage M1 biomarkers (e.g., IL-6, IL-1beta, TNF-alpha, iNOS) in cell culture and in mice. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 103-107 29040966-7 2017 Our results demonstrated that celastrol might control macrophage polarization through modulating the cross-talk between the following three mechanisms: 1) suppressing LPS-induced activation of MAP kinases (e.g., ERK1/2, p38, JNK) in a concentration dependent manner; 2) attenuating LPS-induced nuclear translocation of NF-kappaB p65 subunit in a time dependent manner; 3) activating Nrf2 and subsequently inducing HO-1 expression. celastrol 30-39 mitogen-activated protein kinase 3 Mus musculus 212-218 29040966-7 2017 Our results demonstrated that celastrol might control macrophage polarization through modulating the cross-talk between the following three mechanisms: 1) suppressing LPS-induced activation of MAP kinases (e.g., ERK1/2, p38, JNK) in a concentration dependent manner; 2) attenuating LPS-induced nuclear translocation of NF-kappaB p65 subunit in a time dependent manner; 3) activating Nrf2 and subsequently inducing HO-1 expression. celastrol 30-39 mitogen-activated protein kinase 14 Mus musculus 220-223 29040966-7 2017 Our results demonstrated that celastrol might control macrophage polarization through modulating the cross-talk between the following three mechanisms: 1) suppressing LPS-induced activation of MAP kinases (e.g., ERK1/2, p38, JNK) in a concentration dependent manner; 2) attenuating LPS-induced nuclear translocation of NF-kappaB p65 subunit in a time dependent manner; 3) activating Nrf2 and subsequently inducing HO-1 expression. celastrol 30-39 mitogen-activated protein kinase 8 Mus musculus 225-228 29040966-7 2017 Our results demonstrated that celastrol might control macrophage polarization through modulating the cross-talk between the following three mechanisms: 1) suppressing LPS-induced activation of MAP kinases (e.g., ERK1/2, p38, JNK) in a concentration dependent manner; 2) attenuating LPS-induced nuclear translocation of NF-kappaB p65 subunit in a time dependent manner; 3) activating Nrf2 and subsequently inducing HO-1 expression. celastrol 30-39 nuclear factor, erythroid derived 2, like 2 Mus musculus 383-387 29040966-7 2017 Our results demonstrated that celastrol might control macrophage polarization through modulating the cross-talk between the following three mechanisms: 1) suppressing LPS-induced activation of MAP kinases (e.g., ERK1/2, p38, JNK) in a concentration dependent manner; 2) attenuating LPS-induced nuclear translocation of NF-kappaB p65 subunit in a time dependent manner; 3) activating Nrf2 and subsequently inducing HO-1 expression. celastrol 30-39 heme oxygenase 1 Mus musculus 414-418 29040966-8 2017 HO-1 inhibitor SnPP diminished the inhibitory effects of celastrol on the activation of NF-kappaB pathway and the pro-inflammatory M1 macrophage polarization. celastrol 57-66 heme oxygenase 1 Mus musculus 0-4 28935193-0 2017 Celastrol inhibits hepatitis C virus replication by upregulating heme oxygenase-1 via the JNK MAPK/Nrf2 pathway in human hepatoma cells. celastrol 0-9 NFE2 like bZIP transcription factor 2 Homo sapiens 99-103 28935193-1 2017 BACKGROUND AND PURPOSE: Celastrol, a quinone methide triterpene isolated from the root extracts of Tripterygium wilfordii, can greatly induce the gene expression activity of heme oxygenase-1 (HO-1) to achieve disease prevention and control. celastrol 24-33 heme oxygenase 1 Homo sapiens 192-196 28935193-10 2017 These antiviral effects were abrogated by treatment with the HO-1-specific inhibitor SnMP or silencing of HO-1 expression by transfection of shRNA, which indicates that HO-1 induction contributes to the anti-HCV activity of celastrol. celastrol 224-233 heme oxygenase 1 Homo sapiens 61-65 28935193-10 2017 These antiviral effects were abrogated by treatment with the HO-1-specific inhibitor SnMP or silencing of HO-1 expression by transfection of shRNA, which indicates that HO-1 induction contributes to the anti-HCV activity of celastrol. celastrol 224-233 heme oxygenase 1 Homo sapiens 106-110 28935193-5 2017 The anti-HCV mechanism of celastrol targeting HO-1 expression was clarified using specific inhibitors against several signaling pathways. celastrol 26-35 heme oxygenase 1 Homo sapiens 46-50 28935193-10 2017 These antiviral effects were abrogated by treatment with the HO-1-specific inhibitor SnMP or silencing of HO-1 expression by transfection of shRNA, which indicates that HO-1 induction contributes to the anti-HCV activity of celastrol. celastrol 224-233 heme oxygenase 1 Homo sapiens 106-110 28935193-9 2017 Celastrol-induced heme oxygenase 1 (HO-1) expression promoted antiviral interferon responses and inhibition of NS3/4A protease activity, thereby blocking HCV replication. celastrol 0-9 heme oxygenase 1 Homo sapiens 36-40 28935193-11 2017 JNK mitogen-activated protein kinase and nuclear factor erythroid 2-related factor 2 (Nrf2) were confirmed to be involved in the inductive effect of celastrol on HO-1 expression. celastrol 149-158 NFE2 like bZIP transcription factor 2 Homo sapiens 86-90 28878153-8 2017 The expression of several chemokine genes, including CCL2 , CXCL10 , CXCL12 , CCR2 and CXCR4 , was significantly changed after celastrol treatment. celastrol 127-136 C-C motif chemokine ligand 2 Homo sapiens 53-57 28935193-11 2017 JNK mitogen-activated protein kinase and nuclear factor erythroid 2-related factor 2 (Nrf2) were confirmed to be involved in the inductive effect of celastrol on HO-1 expression. celastrol 149-158 heme oxygenase 1 Homo sapiens 162-166 28878153-8 2017 The expression of several chemokine genes, including CCL2 , CXCL10 , CXCL12 , CCR2 and CXCR4 , was significantly changed after celastrol treatment. celastrol 127-136 C-X-C motif chemokine ligand 10 Homo sapiens 60-66 28878153-8 2017 The expression of several chemokine genes, including CCL2 , CXCL10 , CXCL12 , CCR2 and CXCR4 , was significantly changed after celastrol treatment. celastrol 127-136 C-X-C motif chemokine ligand 12 Homo sapiens 69-75 28878153-8 2017 The expression of several chemokine genes, including CCL2 , CXCL10 , CXCL12 , CCR2 and CXCR4 , was significantly changed after celastrol treatment. celastrol 127-136 C-C motif chemokine receptor 2 Homo sapiens 78-82 28878153-8 2017 The expression of several chemokine genes, including CCL2 , CXCL10 , CXCL12 , CCR2 and CXCR4 , was significantly changed after celastrol treatment. celastrol 127-136 C-X-C motif chemokine receptor 4 Homo sapiens 87-92 28789395-6 2017 The level of cleaved caspases-3, -8, and -9 and poly (ADP-ribose) polymerase 1 increased in cells treated with celastrol. celastrol 111-120 poly(ADP-ribose) polymerase 1 Homo sapiens 21-78 31966802-7 2017 However, celastrol pre-treatment compromised the increased MPO, MDA, TNF-alpha, IL-1beta, IL-6 (all P<0.01) and significantly increased SOD (P=0.035<0.05) and IL-10 (P<0.01). celastrol 9-18 myeloperoxidase Mus musculus 59-62 31966802-7 2017 However, celastrol pre-treatment compromised the increased MPO, MDA, TNF-alpha, IL-1beta, IL-6 (all P<0.01) and significantly increased SOD (P=0.035<0.05) and IL-10 (P<0.01). celastrol 9-18 tumor necrosis factor Mus musculus 69-78 31966802-7 2017 However, celastrol pre-treatment compromised the increased MPO, MDA, TNF-alpha, IL-1beta, IL-6 (all P<0.01) and significantly increased SOD (P=0.035<0.05) and IL-10 (P<0.01). celastrol 9-18 interleukin 1 alpha Mus musculus 80-88 31966802-7 2017 However, celastrol pre-treatment compromised the increased MPO, MDA, TNF-alpha, IL-1beta, IL-6 (all P<0.01) and significantly increased SOD (P=0.035<0.05) and IL-10 (P<0.01). celastrol 9-18 interleukin 6 Mus musculus 90-94 31966802-7 2017 However, celastrol pre-treatment compromised the increased MPO, MDA, TNF-alpha, IL-1beta, IL-6 (all P<0.01) and significantly increased SOD (P=0.035<0.05) and IL-10 (P<0.01). celastrol 9-18 interleukin 10 Mus musculus 165-170 27891586-0 2017 Celastrol Attenuates Cadmium-Induced Neuronal Apoptosis via Inhibiting Ca2+ -CaMKII-Dependent Akt/mTOR Pathway. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 94-97 27891586-0 2017 Celastrol Attenuates Cadmium-Induced Neuronal Apoptosis via Inhibiting Ca2+ -CaMKII-Dependent Akt/mTOR Pathway. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 98-102 27891586-2 2017 Recently, we have shown that celastrol prevents Cd-induced neuronal cell death partially by suppressing Akt/mTOR pathway. celastrol 29-38 AKT serine/threonine kinase 1 Homo sapiens 104-107 27891586-2 2017 Recently, we have shown that celastrol prevents Cd-induced neuronal cell death partially by suppressing Akt/mTOR pathway. celastrol 29-38 mechanistic target of rapamycin kinase Homo sapiens 108-112 27891586-5 2017 Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol"s prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 64-67 27891586-5 2017 Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol"s prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 77-81 27891586-5 2017 Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol"s prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 108-111 27891586-5 2017 Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol"s prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 108-111 27891586-5 2017 Celastrol prevented Cd-induced neuronal apoptosis by inhibiting Akt-mediated mTOR pathway, as inhibition of Akt with Akt inhibitor X or ectopic expression of dominant negative Akt reinforced celastrol"s prevention of Cd-induced phosphorylation of S6K1/4E-BP1 and cell apoptosis. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 108-111 27891586-6 2017 Furthermore, chelating intracellular Ca2+ with BAPTA/AM or preventing [Ca2+ ]i elevation using EGTA potentiated celastrol"s repression of Cd-induced [Ca2+ ]i elevation and consequential activation of Akt/mTOR pathway and cell apoptosis. celastrol 112-121 AKT serine/threonine kinase 1 Homo sapiens 200-203 27891586-6 2017 Furthermore, chelating intracellular Ca2+ with BAPTA/AM or preventing [Ca2+ ]i elevation using EGTA potentiated celastrol"s repression of Cd-induced [Ca2+ ]i elevation and consequential activation of Akt/mTOR pathway and cell apoptosis. celastrol 112-121 mechanistic target of rapamycin kinase Homo sapiens 204-208 27891586-8 2017 Inhibiting CaMKII with KN93 or silencing CaMKII attenuated Cd activation of Akt/mTOR pathway and cell apoptosis, and this was strengthened by celastrol. celastrol 142-151 AKT serine/threonine kinase 1 Homo sapiens 76-79 27891586-8 2017 Inhibiting CaMKII with KN93 or silencing CaMKII attenuated Cd activation of Akt/mTOR pathway and cell apoptosis, and this was strengthened by celastrol. celastrol 142-151 mechanistic target of rapamycin kinase Homo sapiens 80-84 27891586-9 2017 Taken together, these data demonstrate that celastrol attenuates Cd-induced neuronal apoptosis via inhibiting Ca2+ -CaMKII-dependent Akt/mTOR pathway. celastrol 44-53 AKT serine/threonine kinase 1 Homo sapiens 133-136 27891586-9 2017 Taken together, these data demonstrate that celastrol attenuates Cd-induced neuronal apoptosis via inhibiting Ca2+ -CaMKII-dependent Akt/mTOR pathway. celastrol 44-53 mechanistic target of rapamycin kinase Homo sapiens 137-141 28789395-8 2017 Celastrol induced an increase in Fas, Fas-associated via death domain, TNF receptor superfamily members (TNRSF) 1A and 10B, and TNFRSF1A associated via death domain, and induced a dose-dependent reduction in mitochondrial membrane potential. celastrol 0-9 TNF receptor superfamily member 1A Homo sapiens 71-122 28789395-8 2017 Celastrol induced an increase in Fas, Fas-associated via death domain, TNF receptor superfamily members (TNRSF) 1A and 10B, and TNFRSF1A associated via death domain, and induced a dose-dependent reduction in mitochondrial membrane potential. celastrol 0-9 TNF receptor superfamily member 1A Homo sapiens 128-136 28789395-9 2017 Celastrol inhibited activation of mitogen-activated protein kinase (MAPK) 1/3 and 14, and induced MAPK 8/9 activation. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 98-104 28389259-8 2017 Celastrol increased the expressions of Beclin 1 and Vps 34, promoted the up-regulation of Atg5-Atg12-16 formation and enhanced the lipidation of LC3I to LC3II suggesting induction of autophagy by celastrol provide protection against lung fibrosis. celastrol 0-9 beclin 1 Rattus norvegicus 39-47 28389259-8 2017 Celastrol increased the expressions of Beclin 1 and Vps 34, promoted the up-regulation of Atg5-Atg12-16 formation and enhanced the lipidation of LC3I to LC3II suggesting induction of autophagy by celastrol provide protection against lung fibrosis. celastrol 0-9 autophagy related 5 Rattus norvegicus 90-94 28389259-9 2017 Further, we revealed that celastrol activates autophagy by inhibiting PI3K/Akt mediated mTOR expression. celastrol 26-35 AKT serine/threonine kinase 1 Rattus norvegicus 75-78 28389259-9 2017 Further, we revealed that celastrol activates autophagy by inhibiting PI3K/Akt mediated mTOR expression. celastrol 26-35 mechanistic target of rapamycin kinase Rattus norvegicus 88-92 28389259-10 2017 In addition, we show evidences that lack of autophagy leads to accumulation of p62, an autophagy adaptor protein that is degraded by celastrol. celastrol 133-142 KH RNA binding domain containing, signal transduction associated 1 Rattus norvegicus 79-82 28458159-0 2017 Celastrol reduces IL-1beta induced matrix catabolism, oxidative stress and inflammation in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration in vivo. celastrol 0-9 interleukin 1 beta Homo sapiens 18-26 28621943-9 2017 Two compounds, sanguinarine (1) and celastrol (2), were found to be cytostatic against lung and prostate cancer cell lines and cytotoxic against prostate cancer cell lines in vitro, although the dependence of RGS17 on these phenomena remains elusive, a result that is perhaps not surprising given the multimodal cytostatic and cytotoxic activities of many natural products. celastrol 36-45 regulator of G protein signaling 17 Homo sapiens 209-214 28458159-3 2017 In this study, we evaluated the effect of celastrol on IDD in IL-1beta treated human nucleus pulposus cells in vitro as well as in puncture induced rat IDD model in vivo. celastrol 42-51 interleukin 1 beta Homo sapiens 62-70 28458159-6 2017 Together, our study demonstrates that celastrol could reduce IL-1beta induced matrix catabolism, oxidative stress and inflammation in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration in vivo, which shows its potential to be a therapeutic drug for IDD. celastrol 38-47 interleukin 1 beta Homo sapiens 61-69 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 matrix metallopeptidase 3 Rattus norvegicus 77-89 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 ADAM metallopeptidase with thrombospondin type 1 motif, 4 Rattus norvegicus 91-99 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 cytochrome c oxidase II, mitochondrial Rattus norvegicus 131-136 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 nitric oxide synthase 2 Rattus norvegicus 138-142 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 interleukin 6 Rattus norvegicus 174-178 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 tumor necrosis factor Rattus norvegicus 180-185 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 interleukin 1 beta Rattus norvegicus 198-206 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 NFKB inhibitor alpha Rattus norvegicus 258-270 28458159-4 2017 Our results showed that celastrol reduced the expression of catabolic genes (MMP-3, 9, 13, ADAMTS-4, 5), oxidative stress factors (COX-2, iNOS) and pro-inflammatory factors (IL-6, TNF-a) induced by IL-1beta in nucleus pulposus cells, also phosphorylation of IkappaBalpha and p65 were attenuated by celastrol, indicating NF-kappaB pathway was inhibited by celastrol in nucleus pulposus cells. celastrol 24-33 synaptotagmin 1 Rattus norvegicus 275-278 28673005-8 2017 At the molecular level, celastrol blocked the canonical NF-kappaB pathway by inhibiting IkappaBalpha phosphorylation, and preventing IkappaBalpha degradation and p65 accumulation. celastrol 24-33 NFKB inhibitor alpha Homo sapiens 88-100 28673005-8 2017 At the molecular level, celastrol blocked the canonical NF-kappaB pathway by inhibiting IkappaBalpha phosphorylation, and preventing IkappaBalpha degradation and p65 accumulation. celastrol 24-33 NFKB inhibitor alpha Homo sapiens 133-145 28673005-8 2017 At the molecular level, celastrol blocked the canonical NF-kappaB pathway by inhibiting IkappaBalpha phosphorylation, and preventing IkappaBalpha degradation and p65 accumulation. celastrol 24-33 RELA proto-oncogene, NF-kB subunit Homo sapiens 162-165 28673005-9 2017 Furthermore, the expression and activity of the NF-kappaB target protein MMP-9, but not MMP-2, were inhibited by celastrol. celastrol 113-122 matrix metallopeptidase 9 Homo sapiens 73-78 28435131-5 2017 The results indicated that both celastrol and BBG pretreatments, especially when combined together, curbed APAP-induced hepatocellular injury (ALT, AST and LDH) and death (necrosis and apoptosis). celastrol 32-41 glutamic pyruvic transaminase, soluble Mus musculus 143-146 28978034-0 2017 Celastrol ameliorates inflammation through inhibition of NLRP3 inflammasome activation. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 57-62 28978034-3 2017 Here, we show that celastrol abolishes the NLRP3 inflammasome activation, inhibits subsequent caspase-1 activation and IL-1beta secretion both in vitro and in vivo. celastrol 19-28 NLR family pyrin domain containing 3 Homo sapiens 43-48 28978034-3 2017 Here, we show that celastrol abolishes the NLRP3 inflammasome activation, inhibits subsequent caspase-1 activation and IL-1beta secretion both in vitro and in vivo. celastrol 19-28 caspase 1 Homo sapiens 94-103 28978034-3 2017 Here, we show that celastrol abolishes the NLRP3 inflammasome activation, inhibits subsequent caspase-1 activation and IL-1beta secretion both in vitro and in vivo. celastrol 19-28 interleukin 1 beta Homo sapiens 119-127 28978034-4 2017 Notably, interruption of ASC oligomerization and autophagy activation are involved in NLRP3 inflammasome inactivation by celastrol. celastrol 121-130 PYD and CARD domain containing Homo sapiens 25-28 28978034-4 2017 Notably, interruption of ASC oligomerization and autophagy activation are involved in NLRP3 inflammasome inactivation by celastrol. celastrol 121-130 NLR family pyrin domain containing 3 Homo sapiens 86-91 28978034-5 2017 Importantly, in vivo results indicate that celastrol attenuates NLRP3 inflammasome-dependent inflammation diseases via autophagy-related pathway. celastrol 43-52 NLR family pyrin domain containing 3 Homo sapiens 64-69 28978034-6 2017 Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases. celastrol 24-33 NLR family pyrin domain containing 3 Homo sapiens 53-58 28978034-6 2017 Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases. celastrol 24-33 NLR family pyrin domain containing 3 Homo sapiens 142-147 28978034-6 2017 Our results thus reveal celastrol as an inhibitor of NLRP3 inflammasome, implying the potential for clinical use of celastrol in treatment of NLRP3 inflammasome-driven inflammatory diseases. celastrol 116-125 NLR family pyrin domain containing 3 Homo sapiens 142-147 28435131-5 2017 The results indicated that both celastrol and BBG pretreatments, especially when combined together, curbed APAP-induced hepatocellular injury (ALT, AST and LDH) and death (necrosis and apoptosis). celastrol 32-41 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 148-151 28730769-1 2017 PURPOSE: To investigate the effect and related molecular mechanisms of lapatinib/celastrol combination or single-agent treatment in HER2/neu-overexpressing MDA-MB-453 breast cancer cells. celastrol 81-90 erb-b2 receptor tyrosine kinase 2 Homo sapiens 137-140 28730769-8 2017 RESULTS: Combination celastrol and lapatinib produced strong synergy in growth inhibition and apoptosis in comparison to single-agent treatment in HER2/neu-overexpressing MDA-MB-453 cells. celastrol 21-30 erb-b2 receptor tyrosine kinase 2 Homo sapiens 152-155 28730769-0 2017 Downregulation and subcellular distribution of HER2 involved in MDA-MB-453 breast cancer cell apoptosis induced by lapatinib/celastrol combination. celastrol 125-134 erb-b2 receptor tyrosine kinase 2 Homo sapiens 47-51 28730769-9 2017 Interestingly, compared with celastrol treatment alone, lapatinib/celastrol combination induced more HER2 membrane protein downregulation and ectopic to cytoplasm and nucleus in MDA-MB-453 cells. celastrol 66-75 erb-b2 receptor tyrosine kinase 2 Homo sapiens 101-105 28730769-1 2017 PURPOSE: To investigate the effect and related molecular mechanisms of lapatinib/celastrol combination or single-agent treatment in HER2/neu-overexpressing MDA-MB-453 breast cancer cells. celastrol 81-90 erb-b2 receptor tyrosine kinase 2 Homo sapiens 132-136 28730769-10 2017 CONCLUSION: The combination of celastrol and lapatinib could be used as a novel combination regimen which provides a strong anticancer synergy in the treatment of HER2/neu-overexpressing cancer cells. celastrol 31-40 erb-b2 receptor tyrosine kinase 2 Homo sapiens 163-167 28730769-10 2017 CONCLUSION: The combination of celastrol and lapatinib could be used as a novel combination regimen which provides a strong anticancer synergy in the treatment of HER2/neu-overexpressing cancer cells. celastrol 31-40 erb-b2 receptor tyrosine kinase 2 Homo sapiens 168-171 28522217-0 2017 Celastrol inhibits chondrosarcoma proliferation, migration and invasion through suppression CIP2A/c-MYC signaling pathway. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 92-97 28522217-0 2017 Celastrol inhibits chondrosarcoma proliferation, migration and invasion through suppression CIP2A/c-MYC signaling pathway. celastrol 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 98-103 28522217-3 2017 F.) called celastrol can directly bound CIP2A protein and effectively inhibit cell proliferation and induce apoptosis in several cancer cells. celastrol 11-20 cellular inhibitor of PP2A Homo sapiens 40-45 28522217-7 2017 In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2. celastrol 13-22 cellular inhibitor of PP2A Homo sapiens 51-56 28522217-7 2017 In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2. celastrol 13-22 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 28522217-7 2017 In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2. celastrol 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 99-102 28522217-7 2017 In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2. celastrol 13-22 caspase 8 Homo sapiens 107-116 28522217-7 2017 In addition, celastrol inhibited the expression of CIP2A, c-MYC, and suppressed apoptotic proteins BAX and caspase-8 in human CS cells, on the other hand, it induced the expression of antiapoptotic protein Bcl-2. celastrol 13-22 BCL2 apoptosis regulator Homo sapiens 206-211 28522217-9 2017 To sum up, we found that celastrol had effects on inhibiting proliferation, migration, invasion and inducing apoptosis through suppression CIP2A/c-MYC signaling pathway in vitro, which may provide a new therapeutic regimen for CS. celastrol 25-34 cellular inhibitor of PP2A Homo sapiens 139-144 28522217-9 2017 To sum up, we found that celastrol had effects on inhibiting proliferation, migration, invasion and inducing apoptosis through suppression CIP2A/c-MYC signaling pathway in vitro, which may provide a new therapeutic regimen for CS. celastrol 25-34 MYC proto-oncogene, bHLH transcription factor Homo sapiens 145-150 28459364-10 2017 In conclusion, our results suggest that celastrol induces cytotoxicity through involvement of Bcl2 family proteins and death receptor, and modulation of phospho-NF-kappaB, Akt, and mitogen-activated protein kinase in association with endoplasmic reticulum stress and reactive oxygen species production in anaplastic thyroid carcinoma cells. celastrol 40-49 BCL2 apoptosis regulator Homo sapiens 94-98 28459364-10 2017 In conclusion, our results suggest that celastrol induces cytotoxicity through involvement of Bcl2 family proteins and death receptor, and modulation of phospho-NF-kappaB, Akt, and mitogen-activated protein kinase in association with endoplasmic reticulum stress and reactive oxygen species production in anaplastic thyroid carcinoma cells. celastrol 40-49 AKT serine/threonine kinase 1 Homo sapiens 172-175 28129433-5 2017 Also, N-acetyl-l-cysteine, a ROS scavenger, potentiated celastrol"s inhibition of the events in the cells triggered by Cd, implying neuroprotection by celastrol via blocking Cd-evoked NOX2-derived ROS. celastrol 56-65 cytochrome b-245 beta chain Rattus norvegicus 184-188 28129433-0 2017 Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 0-9 cytochrome b-245 beta chain Rattus norvegicus 65-69 28388439-0 2017 Celastrol-Induced Nur77 Interaction with TRAF2 Alleviates Inflammation by Promoting Mitochondrial Ubiquitination and Autophagy. celastrol 0-9 nuclear receptor subfamily 4 group A member 1 Homo sapiens 18-23 28388439-0 2017 Celastrol-Induced Nur77 Interaction with TRAF2 Alleviates Inflammation by Promoting Mitochondrial Ubiquitination and Autophagy. celastrol 0-9 TNF receptor associated factor 2 Homo sapiens 41-46 28388439-3 2017 Here, we report that celastrol, a potent anti-inflammatory pentacyclic triterpene, binds Nur77 to inhibit inflammation and induce autophagy in a Nur77-dependent manner. celastrol 21-30 nuclear receptor subfamily 4 group A member 1 Homo sapiens 89-94 28388439-3 2017 Here, we report that celastrol, a potent anti-inflammatory pentacyclic triterpene, binds Nur77 to inhibit inflammation and induce autophagy in a Nur77-dependent manner. celastrol 21-30 nuclear receptor subfamily 4 group A member 1 Homo sapiens 145-150 28388439-4 2017 Celastrol promotes Nur77 translocation from the nucleus to mitochondria, where it interacts with tumor necrosis factor receptor-associated factor 2 (TRAF2), a scaffold protein and E3 ubiquitin ligase important for inflammatory signaling. celastrol 0-9 nuclear receptor subfamily 4 group A member 1 Homo sapiens 19-24 28388439-4 2017 Celastrol promotes Nur77 translocation from the nucleus to mitochondria, where it interacts with tumor necrosis factor receptor-associated factor 2 (TRAF2), a scaffold protein and E3 ubiquitin ligase important for inflammatory signaling. celastrol 0-9 TNF receptor associated factor 2 Homo sapiens 97-147 28388439-4 2017 Celastrol promotes Nur77 translocation from the nucleus to mitochondria, where it interacts with tumor necrosis factor receptor-associated factor 2 (TRAF2), a scaffold protein and E3 ubiquitin ligase important for inflammatory signaling. celastrol 0-9 TNF receptor associated factor 2 Homo sapiens 149-154 28388439-7 2017 Together, our results identify Nur77 as a critical intracellular target for celastrol and unravel a mechanism of Nur77-dependent clearance of inflamed mitochondria to alleviate inflammation. celastrol 76-85 nuclear receptor subfamily 4 group A member 1 Homo sapiens 31-36 28397045-0 2017 Celastrol protects TGF-beta1-induced endothelial-mesenchymal transition. celastrol 0-9 transforming growth factor beta 1 Homo sapiens 19-28 28397045-2 2017 In this study, the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-beta1 (TGF-beta1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated. celastrol 55-64 transforming growth factor beta 1 Homo sapiens 74-106 28397045-2 2017 In this study, the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-beta1 (TGF-beta1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated. celastrol 55-64 transforming growth factor beta 1 Homo sapiens 108-117 28397045-2 2017 In this study, the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-beta1 (TGF-beta1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated. celastrol 66-69 transforming growth factor beta 1 Homo sapiens 74-106 28397045-2 2017 In this study, the effects and molecular mechanisms of celastrol (CEL) on transforming growth factor-beta1 (TGF-beta1)-induced EndMT in human umbilical vein endothelial (HUVEC-12) cells were investigated. celastrol 66-69 transforming growth factor beta 1 Homo sapiens 108-117 28397045-6 2017 The in vitro scratch assay showed that CEL inhibited the migration capacity of the transitioned endothelial cells induced by TGF-beta1. celastrol 39-42 transforming growth factor beta 1 Homo sapiens 125-134 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 transforming growth factor beta 1 Homo sapiens 144-153 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 snail family transcriptional repressor 1 Homo sapiens 262-268 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 twist family bHLH transcription factor 1 Homo sapiens 270-276 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 twist family bHLH transcription factor 2 Homo sapiens 278-284 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 zinc finger E-box binding homeobox 1 Homo sapiens 286-290 28397045-7 2017 Further experiments showed that the beneficial effect of CEL on blocking the EndMT in HUVEC-12 cells was associated with the suppression of the TGF-beta1/Smads signalling pathway, which was also confirmed by the inhibition of its downstream transcription factor snail1, twist1, twist2, ZEB1 and ZEB2. celastrol 57-60 zinc finger E-box binding homeobox 2 Homo sapiens 295-299 28129433-0 2017 Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 0-9 protein phosphatase 5, catalytic subunit Rattus norvegicus 92-95 28129433-0 2017 Celastrol ameliorates Cd-induced neuronal apoptosis by targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 0-9 mitogen-activated protein kinase 8 Rattus norvegicus 96-99 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. celastrol 189-198 mitogen-activated protein kinase 8 Rattus norvegicus 55-78 28129433-2 2017 Recently, we have reported that cadmium (Cd) activates c-Jun N-terminal kinase (JNK) pathway leading to neuronal cell death by inducing ROS inactivation of protein phosphatase 5 (PP5), and celastrol prevents Cd-activated JNK pathway against neuronal apoptosis. celastrol 189-198 mitogen-activated protein kinase 8 Rattus norvegicus 80-83 28129433-3 2017 Therefore, we hypothesized that celastrol could hinder Cd induction of ROS-dependent PP5-JNK signaling pathway from apoptosis in neuronal cells. celastrol 32-41 protein phosphatase 5, catalytic subunit Rattus norvegicus 85-88 28129433-3 2017 Therefore, we hypothesized that celastrol could hinder Cd induction of ROS-dependent PP5-JNK signaling pathway from apoptosis in neuronal cells. celastrol 32-41 mitogen-activated protein kinase 8 Rattus norvegicus 89-92 28129433-4 2017 Here, we show that celastrol attenuated Cd-induced expression of NADPH oxidase 2 (NOX2) and its regulatory proteins (p22phox , p40phox , p47phox , p67phox , and Rac1), as well as the generation of ROS in PC12 cells and primary neurons. celastrol 19-28 cytochrome b-245 beta chain Rattus norvegicus 65-80 28129433-4 2017 Here, we show that celastrol attenuated Cd-induced expression of NADPH oxidase 2 (NOX2) and its regulatory proteins (p22phox , p40phox , p47phox , p67phox , and Rac1), as well as the generation of ROS in PC12 cells and primary neurons. celastrol 19-28 cytochrome b-245 beta chain Rattus norvegicus 82-86 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 31-40 protein phosphatase 5, catalytic subunit Rattus norvegicus 75-78 28129433-4 2017 Here, we show that celastrol attenuated Cd-induced expression of NADPH oxidase 2 (NOX2) and its regulatory proteins (p22phox , p40phox , p47phox , p67phox , and Rac1), as well as the generation of ROS in PC12 cells and primary neurons. celastrol 19-28 cytochrome b-245 alpha chain Rattus norvegicus 117-124 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 31-40 mitogen-activated protein kinase 8 Rattus norvegicus 96-99 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 31-40 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-4 2017 Here, we show that celastrol attenuated Cd-induced expression of NADPH oxidase 2 (NOX2) and its regulatory proteins (p22phox , p40phox , p47phox , p67phox , and Rac1), as well as the generation of ROS in PC12 cells and primary neurons. celastrol 19-28 neutrophil cytosolic factor 1 Rattus norvegicus 137-144 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 31-40 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 31-40 mitogen-activated protein kinase 8 Rattus norvegicus 321-324 28129433-4 2017 Here, we show that celastrol attenuated Cd-induced expression of NADPH oxidase 2 (NOX2) and its regulatory proteins (p22phox , p40phox , p47phox , p67phox , and Rac1), as well as the generation of ROS in PC12 cells and primary neurons. celastrol 19-28 Rac family small GTPase 1 Rattus norvegicus 161-165 28129433-9 2017 These findings indicate that celastrol ameliorates Cd-induced neuronal apoptosis via targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 29-38 protein phosphatase 5, catalytic subunit Rattus norvegicus 122-125 28129433-9 2017 These findings indicate that celastrol ameliorates Cd-induced neuronal apoptosis via targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 29-38 mitogen-activated protein kinase 8 Rattus norvegicus 126-129 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 135-144 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 135-144 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 135-144 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-6 2017 Further research revealed that celastrol was involved in the regulation of PP5 inactivation and JNK/c-Jun activation induced by Cd, as celastrol prevented Cd from reducing PP5 expression, and over-expression of wild-type PP5 or dominant negative c-Jun strengthened celastrol"s inhibition of Cd-induced phosphorylation of JNK and/or c-Jun, as well as apoptosis in neuronal cells. celastrol 135-144 protein phosphatase 5, catalytic subunit Rattus norvegicus 172-175 28129433-7 2017 Of importance, inhibiting NOX2 with apocynin or silencing NOX2 by RNA interference enhanced the inhibitory effects of celastrol on Cd-induced inactivation of PP5, activation of JNK/c-Jun, ROS, and apoptosis in the cells. celastrol 118-127 cytochrome b-245 beta chain Rattus norvegicus 26-30 28129433-7 2017 Of importance, inhibiting NOX2 with apocynin or silencing NOX2 by RNA interference enhanced the inhibitory effects of celastrol on Cd-induced inactivation of PP5, activation of JNK/c-Jun, ROS, and apoptosis in the cells. celastrol 118-127 cytochrome b-245 beta chain Rattus norvegicus 58-62 28129433-7 2017 Of importance, inhibiting NOX2 with apocynin or silencing NOX2 by RNA interference enhanced the inhibitory effects of celastrol on Cd-induced inactivation of PP5, activation of JNK/c-Jun, ROS, and apoptosis in the cells. celastrol 118-127 protein phosphatase 5, catalytic subunit Rattus norvegicus 158-161 28129433-7 2017 Of importance, inhibiting NOX2 with apocynin or silencing NOX2 by RNA interference enhanced the inhibitory effects of celastrol on Cd-induced inactivation of PP5, activation of JNK/c-Jun, ROS, and apoptosis in the cells. celastrol 118-127 mitogen-activated protein kinase 8 Rattus norvegicus 177-180 28129433-8 2017 Furthermore, we noticed that expression of wild-type PP5 or dominant negative c-Jun, or pretreatment with JNK inhibitor SP600125 reinforced celastrol"s suppression of Cd-induced NOX2 and its regulatory proteins, and consequential ROS in neuronal cells. celastrol 140-149 protein phosphatase 5, catalytic subunit Rattus norvegicus 53-56 28129433-8 2017 Furthermore, we noticed that expression of wild-type PP5 or dominant negative c-Jun, or pretreatment with JNK inhibitor SP600125 reinforced celastrol"s suppression of Cd-induced NOX2 and its regulatory proteins, and consequential ROS in neuronal cells. celastrol 140-149 mitogen-activated protein kinase 8 Rattus norvegicus 106-109 28129433-8 2017 Furthermore, we noticed that expression of wild-type PP5 or dominant negative c-Jun, or pretreatment with JNK inhibitor SP600125 reinforced celastrol"s suppression of Cd-induced NOX2 and its regulatory proteins, and consequential ROS in neuronal cells. celastrol 140-149 cytochrome b-245 beta chain Rattus norvegicus 178-182 28129433-9 2017 These findings indicate that celastrol ameliorates Cd-induced neuronal apoptosis via targeting NOX2-derived ROS-dependent PP5-JNK signaling pathway. celastrol 29-38 cytochrome b-245 beta chain Rattus norvegicus 95-99 28189063-3 2017 Protective effect of celastrol (1mg/kg, i.p., 1h before CLP) was illustrated after 24h by preventing CLP-induced hepatic histopathological changes and elevation in serum hepatic biomarkers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and gamma aminotransferase (gamma-GT)] without affecting mortality. celastrol 21-30 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 222-248 28161417-0 2017 Celastrol attenuates mitochondrial dysfunction and inflammation in palmitate-mediated insulin resistance in C3A hepatocytes. celastrol 0-9 insulin Homo sapiens 86-93 28161417-2 2017 Celastrol, an anti-inflammatory compound from the root of Tripterygium Wilfordii has been reported to mitigate insulin resistance and inflammation in animal disease models. celastrol 0-9 insulin Homo sapiens 111-118 28161417-4 2017 The present study sought to explore the mechanistic roles of celastrol upon insulin resistance induced by palmitate in C3A human hepatocytes. celastrol 61-70 insulin Homo sapiens 76-83 28161417-8 2017 However, celastrol at the optimum concentration of 30nM was able to reverse these deleterious occasions and protected the cells from mitochondrial dysfunction and insulin resistance. celastrol 9-18 insulin Homo sapiens 163-170 28161417-9 2017 Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. celastrol 59-68 insulin Homo sapiens 109-116 28161417-9 2017 Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. celastrol 59-68 insulin Homo sapiens 194-201 28189063-3 2017 Protective effect of celastrol (1mg/kg, i.p., 1h before CLP) was illustrated after 24h by preventing CLP-induced hepatic histopathological changes and elevation in serum hepatic biomarkers [alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and gamma aminotransferase (gamma-GT)] without affecting mortality. celastrol 21-30 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 250-253 28189063-4 2017 Celastrol anti-inflammatory effect was illustrated by inhibiting increased serum and hepatic mRNA expression of interleukin-6 (IL-6) without affecting IL-10 elevation. celastrol 0-9 interleukin 6 Rattus norvegicus 112-125 28189063-4 2017 Celastrol anti-inflammatory effect was illustrated by inhibiting increased serum and hepatic mRNA expression of interleukin-6 (IL-6) without affecting IL-10 elevation. celastrol 0-9 interleukin 6 Rattus norvegicus 127-131 28189063-5 2017 Furthermore, celastrol inhibited CLP-induced elevations in hepatic mRNA expression of nuclear factor inhibitory protein kappa-B alpha (NFkappaBia), TLR-4, 5-lipoxygenase (5-LOX) and prevented NF-kappaB/p65 nuclear translocation and activation. celastrol 13-22 toll-like receptor 4 Rattus norvegicus 148-153 28189063-5 2017 Furthermore, celastrol inhibited CLP-induced elevations in hepatic mRNA expression of nuclear factor inhibitory protein kappa-B alpha (NFkappaBia), TLR-4, 5-lipoxygenase (5-LOX) and prevented NF-kappaB/p65 nuclear translocation and activation. celastrol 13-22 lysyl oxidase Rattus norvegicus 173-176 28189063-5 2017 Furthermore, celastrol inhibited CLP-induced elevations in hepatic mRNA expression of nuclear factor inhibitory protein kappa-B alpha (NFkappaBia), TLR-4, 5-lipoxygenase (5-LOX) and prevented NF-kappaB/p65 nuclear translocation and activation. celastrol 13-22 synaptotagmin 1 Rattus norvegicus 202-205 28189063-6 2017 In conclusion, celastrol prevented CLP-induced acute hepatic dysfunction through its anti-inflammatory effect by attenuating NF-kappaB activation, TLR-4 and 5-LOX expression with subsequent reduction in pro-inflammatory IL-6. celastrol 15-24 toll-like receptor 4 Rattus norvegicus 147-152 28189063-6 2017 In conclusion, celastrol prevented CLP-induced acute hepatic dysfunction through its anti-inflammatory effect by attenuating NF-kappaB activation, TLR-4 and 5-LOX expression with subsequent reduction in pro-inflammatory IL-6. celastrol 15-24 lysyl oxidase Rattus norvegicus 159-162 28189063-6 2017 In conclusion, celastrol prevented CLP-induced acute hepatic dysfunction through its anti-inflammatory effect by attenuating NF-kappaB activation, TLR-4 and 5-LOX expression with subsequent reduction in pro-inflammatory IL-6. celastrol 15-24 interleukin 6 Rattus norvegicus 220-224 28119074-0 2017 Celastrol attenuates angiotensin II mediated human umbilical vein endothelial cells damage through activation of Nrf2/ERK1/2/Nox2 signal pathway. celastrol 0-9 NFE2 like bZIP transcription factor 2 Homo sapiens 113-117 28119074-0 2017 Celastrol attenuates angiotensin II mediated human umbilical vein endothelial cells damage through activation of Nrf2/ERK1/2/Nox2 signal pathway. celastrol 0-9 cytochrome b-245 beta chain Homo sapiens 125-129 28119074-0 2017 Celastrol attenuates angiotensin II mediated human umbilical vein endothelial cells damage through activation of Nrf2/ERK1/2/Nox2 signal pathway. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 118-124 28119074-6 2017 In contrast, celastrol effectively suppressed reactive oxygen species generation, improved endothelial cell activity, and ameliorated Ang II-mediated HUVEC injury through activation of Nrf2, inhibition of Nox2/AT1 receptor expression, and upregulated phosphorylation of ERK1/2. celastrol 13-22 NFE2 like bZIP transcription factor 2 Homo sapiens 185-189 28119074-6 2017 In contrast, celastrol effectively suppressed reactive oxygen species generation, improved endothelial cell activity, and ameliorated Ang II-mediated HUVEC injury through activation of Nrf2, inhibition of Nox2/AT1 receptor expression, and upregulated phosphorylation of ERK1/2. celastrol 13-22 cytochrome b-245 beta chain Homo sapiens 205-209 28027722-7 2017 These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/NF-kappaB in astrocytes. celastrol 27-36 signal transducer and activator of transcription 1 Homo sapiens 182-187 28119074-6 2017 In contrast, celastrol effectively suppressed reactive oxygen species generation, improved endothelial cell activity, and ameliorated Ang II-mediated HUVEC injury through activation of Nrf2, inhibition of Nox2/AT1 receptor expression, and upregulated phosphorylation of ERK1/2. celastrol 13-22 mitogen-activated protein kinase 3 Homo sapiens 270-276 28119074-7 2017 After treatment with brusatol, a specific inhibitor of Nrf2, the protective effects of celastrol on Ang II-induced damage in HUVECs were remarkably alleviated. celastrol 87-96 NFE2 like bZIP transcription factor 2 Homo sapiens 55-59 28119074-8 2017 Taken together, celastrol-induced activation of Nrf2 and inhibition of NADPH oxidase activity were critical for the inhibition of Ang II-mediated endothelial dysfunction, and demonstrated the potential application of celastrol in CVD therapy. celastrol 16-25 NFE2 like bZIP transcription factor 2 Homo sapiens 48-52 28119074-8 2017 Taken together, celastrol-induced activation of Nrf2 and inhibition of NADPH oxidase activity were critical for the inhibition of Ang II-mediated endothelial dysfunction, and demonstrated the potential application of celastrol in CVD therapy. celastrol 217-226 NFE2 like bZIP transcription factor 2 Homo sapiens 48-52 27910878-0 2017 Lipids: Celastrol protects against fatty liver through SIRT1. celastrol 8-17 sirtuin 1 Homo sapiens 55-60 28027722-0 2017 Celastrol suppresses expression of adhesion molecules and chemokines by inhibiting JNK-STAT1/NF-kappaB activation in poly(I:C)-stimulated astrocytes. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 83-86 27847245-10 2017 This antiviral effect of celastrol was associated with celastrol-induced interferon-alpha (IFN-alpha) expression and was attenuated by a specific inhibitor of the JAK-STAT signaling pathway downstream of IFN-alpha or specific shRNA. celastrol 25-34 interferon alpha Mus musculus 73-89 27847245-10 2017 This antiviral effect of celastrol was associated with celastrol-induced interferon-alpha (IFN-alpha) expression and was attenuated by a specific inhibitor of the JAK-STAT signaling pathway downstream of IFN-alpha or specific shRNA. celastrol 25-34 interferon alpha Mus musculus 91-100 27847245-10 2017 This antiviral effect of celastrol was associated with celastrol-induced interferon-alpha (IFN-alpha) expression and was attenuated by a specific inhibitor of the JAK-STAT signaling pathway downstream of IFN-alpha or specific shRNA. celastrol 25-34 interferon alpha Mus musculus 204-213 27847245-10 2017 This antiviral effect of celastrol was associated with celastrol-induced interferon-alpha (IFN-alpha) expression and was attenuated by a specific inhibitor of the JAK-STAT signaling pathway downstream of IFN-alpha or specific shRNA. celastrol 55-64 interferon alpha Mus musculus 73-89 27847245-10 2017 This antiviral effect of celastrol was associated with celastrol-induced interferon-alpha (IFN-alpha) expression and was attenuated by a specific inhibitor of the JAK-STAT signaling pathway downstream of IFN-alpha or specific shRNA. celastrol 55-64 interferon alpha Mus musculus 91-100 27847245-12 2017 CONCLUSION: Celastrol represents a potential anti-DENV agent that induces IFN-alpha expression and stimulates a downstream antiviral response, making the therapy a promising drug or dietary supplement for the treatment of DENV-infected patients. celastrol 12-21 interferon alpha 1 Homo sapiens 74-83 27764525-0 2017 Celastrol prevents cadmium-induced neuronal cell death by blocking reactive oxygen species-mediated mammalian target of rapamycin pathway. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 100-129 27764525-7 2017 RESULTS: Celastrol attenuated Cd-induced apoptosis by suppressing Cd activation of mTOR, which was attributed to preventing Cd inactivation of AMPK. celastrol 9-18 mechanistic target of rapamycin kinase Homo sapiens 83-87 27764525-7 2017 RESULTS: Celastrol attenuated Cd-induced apoptosis by suppressing Cd activation of mTOR, which was attributed to preventing Cd inactivation of AMPK. celastrol 9-18 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 143-147 27764525-8 2017 Inhibition of AMPK with compound C or expression of dominant negative AMPKalpha prevented celastrol from hindering Cd-induced dephosphorylation of AMPKalpha, activation of mTOR and apoptosis. celastrol 90-99 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 14-18 27764525-8 2017 Inhibition of AMPK with compound C or expression of dominant negative AMPKalpha prevented celastrol from hindering Cd-induced dephosphorylation of AMPKalpha, activation of mTOR and apoptosis. celastrol 90-99 mechanistic target of rapamycin kinase Homo sapiens 172-176 27764525-9 2017 Inhibition of mTOR with rapamycin or knockdown of mTOR potentiated prevention by celastrol, of Cd-induced phosphorylation of p70 S6 kinase 1/eukaryotic initiation factor 4E binding protein 1 and apoptosis. celastrol 81-90 mechanistic target of rapamycin kinase Homo sapiens 14-18 27764525-9 2017 Inhibition of mTOR with rapamycin or knockdown of mTOR potentiated prevention by celastrol, of Cd-induced phosphorylation of p70 S6 kinase 1/eukaryotic initiation factor 4E binding protein 1 and apoptosis. celastrol 81-90 mechanistic target of rapamycin kinase Homo sapiens 50-54 27764525-11 2017 CONCLUSIONS AND IMPLICATIONS: Celastrol prevented the inactivation of AMPK by mitochondrial ROS, thus attenuating Cd-induced mTOR activation and neuronal apoptosis. celastrol 30-39 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 70-74 27764525-11 2017 CONCLUSIONS AND IMPLICATIONS: Celastrol prevented the inactivation of AMPK by mitochondrial ROS, thus attenuating Cd-induced mTOR activation and neuronal apoptosis. celastrol 30-39 mechanistic target of rapamycin kinase Homo sapiens 125-129 28027722-0 2017 Celastrol suppresses expression of adhesion molecules and chemokines by inhibiting JNK-STAT1/NF-kappaB activation in poly(I:C)-stimulated astrocytes. celastrol 0-9 signal transducer and activator of transcription 1 Homo sapiens 87-92 28027722-0 2017 Celastrol suppresses expression of adhesion molecules and chemokines by inhibiting JNK-STAT1/NF-kappaB activation in poly(I:C)-stimulated astrocytes. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 93-102 28027722-4 2017 Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. celastrol 0-9 intercellular adhesion molecule 1 Homo sapiens 94-100 28027722-4 2017 Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. celastrol 0-9 vascular cell adhesion molecule 1 Homo sapiens 101-107 28027722-4 2017 Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. celastrol 0-9 C-C motif chemokine ligand 2 Homo sapiens 133-137 28027722-4 2017 Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. celastrol 0-9 C-X-C motif chemokine ligand 8 Homo sapiens 139-144 28027722-4 2017 Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. celastrol 0-9 C-X-C motif chemokine ligand 10 Homo sapiens 150-156 28027722-7 2017 These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/NF-kappaB in astrocytes. celastrol 27-36 nuclear factor kappa B subunit 1 Homo sapiens 188-197 27273088-7 2016 Celastrol activates heat shock transcription factor 1 (HSF1), the master regulator of Hsp gene transcription, and also exhibits potent anti-inflammatory and anti-oxidant activities. celastrol 0-9 heat shock transcription factor 1 Homo sapiens 20-53 28027722-5 2017 In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. celastrol 13-22 mitogen-activated protein kinase 8 Homo sapiens 80-83 28027722-5 2017 In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. celastrol 13-22 signal transducer and activator of transcription 1 Homo sapiens 93-98 28027722-6 2017 Furthermore, celastrol significantly suppressed poly(I:C)-induced activation of the NF-kappaB signaling pathway. celastrol 13-22 nuclear factor kappa B subunit 1 Homo sapiens 84-93 28027722-7 2017 These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/NF-kappaB in astrocytes. celastrol 27-36 mitogen-activated protein kinase 8 Homo sapiens 173-176 27823626-7 2016 Celastrol induced occludin, claudin-5 and zonula occludens-1 (ZO-1) in endothelial cells. celastrol 0-9 occludin Mus musculus 18-26 27823626-7 2016 Celastrol induced occludin, claudin-5 and zonula occludens-1 (ZO-1) in endothelial cells. celastrol 0-9 claudin 5 Mus musculus 28-37 27823626-7 2016 Celastrol induced occludin, claudin-5 and zonula occludens-1 (ZO-1) in endothelial cells. celastrol 0-9 tight junction protein 1 Mus musculus 42-60 27823626-7 2016 Celastrol induced occludin, claudin-5 and zonula occludens-1 (ZO-1) in endothelial cells. celastrol 0-9 tight junction protein 1 Mus musculus 62-66 27823626-9 2016 Further mechanistic studies revealed that celastrol induced the expression of occludin and ZO-1) via activating MAPKs and PI3K/Akt/mTOR pathway. celastrol 42-51 occludin Mus musculus 78-86 27823626-9 2016 Further mechanistic studies revealed that celastrol induced the expression of occludin and ZO-1) via activating MAPKs and PI3K/Akt/mTOR pathway. celastrol 42-51 tight junction protein 1 Mus musculus 91-95 27823626-9 2016 Further mechanistic studies revealed that celastrol induced the expression of occludin and ZO-1) via activating MAPKs and PI3K/Akt/mTOR pathway. celastrol 42-51 thymoma viral proto-oncogene 1 Mus musculus 127-130 27823626-9 2016 Further mechanistic studies revealed that celastrol induced the expression of occludin and ZO-1) via activating MAPKs and PI3K/Akt/mTOR pathway. celastrol 42-51 mechanistic target of rapamycin kinase Mus musculus 131-135 27823626-10 2016 We also observed that celastrol regulated claudin-5 expression through different mechanisms. celastrol 22-31 claudin 5 Mus musculus 42-51 27647369-0 2016 Optimization and biological evaluation of celastrol derivatives as Hsp90-Cdc37 interaction disruptors with improved druglike properties. celastrol 42-51 heat shock protein 90 alpha family class A member 1 Homo sapiens 67-72 27647369-0 2016 Optimization and biological evaluation of celastrol derivatives as Hsp90-Cdc37 interaction disruptors with improved druglike properties. celastrol 42-51 cell division cycle 37, HSP90 cochaperone Homo sapiens 73-78 27647369-5 2016 Celastrol, as a natural product, can disrupt the Hsp90-Cdc37 interaction and induce degradation of kinase clients. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 49-54 27647369-5 2016 Celastrol, as a natural product, can disrupt the Hsp90-Cdc37 interaction and induce degradation of kinase clients. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 55-60 27647369-6 2016 The study conducted here attempted to elucidate the structure-activity relationship of celastrol derivatives as Hsp90-Cdc37 disruptors and to improve the druglike properties. celastrol 87-96 heat shock protein 90 alpha family class A member 1 Homo sapiens 112-117 27647369-6 2016 The study conducted here attempted to elucidate the structure-activity relationship of celastrol derivatives as Hsp90-Cdc37 disruptors and to improve the druglike properties. celastrol 87-96 cell division cycle 37, HSP90 cochaperone Homo sapiens 118-123 27900015-0 2016 Celastrol negatively regulates cell invasion and migration ability of human osteosarcoma via downregulation of the PI3K/Akt/NF-kappaB signaling pathway in vitro. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 120-123 27900015-0 2016 Celastrol negatively regulates cell invasion and migration ability of human osteosarcoma via downregulation of the PI3K/Akt/NF-kappaB signaling pathway in vitro. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 124-133 27900015-9 2016 We observed that the PI3K/Akt/NF-kappaB signaling pathway was inhibited following Celastrol treatment. celastrol 82-91 AKT serine/threonine kinase 1 Homo sapiens 26-29 27900015-9 2016 We observed that the PI3K/Akt/NF-kappaB signaling pathway was inhibited following Celastrol treatment. celastrol 82-91 nuclear factor kappa B subunit 1 Homo sapiens 30-39 27900015-10 2016 In addition, the expression levels of MMP-2 and -9 proteins were also reduced significantly following Celastrol treatment. celastrol 102-111 matrix metallopeptidase 2 Homo sapiens 38-50 27900015-11 2016 Therefore, we confirmed that Celastrol suppressed osteosarcoma U-2OS cell metastasis via downregulation of the PI3K/Akt/NF-kappaB signaling pathway in vitro. celastrol 29-38 AKT serine/threonine kinase 1 Homo sapiens 116-119 27900015-11 2016 Therefore, we confirmed that Celastrol suppressed osteosarcoma U-2OS cell metastasis via downregulation of the PI3K/Akt/NF-kappaB signaling pathway in vitro. celastrol 29-38 nuclear factor kappa B subunit 1 Homo sapiens 120-129 27597642-0 2016 Celastrol modulates inflammation through inhibition of the catalytic activity of mediators of arachidonic acid pathway: Secretory phospholipase A2 group IIA, 5-lipoxygenase and cyclooxygenase-2. celastrol 0-9 arachidonate 5-lipoxygenase Homo sapiens 158-172 27597642-0 2016 Celastrol modulates inflammation through inhibition of the catalytic activity of mediators of arachidonic acid pathway: Secretory phospholipase A2 group IIA, 5-lipoxygenase and cyclooxygenase-2. celastrol 0-9 prostaglandin-endoperoxide synthase 2 Homo sapiens 177-193 27597642-5 2016 We provide the first evidence for celastrol"s ability to inhibit the catalytic activity of sPLA2IIA, 5-LOX and COX-2 enzymes. celastrol 34-43 phospholipase A2, group IIA (platelets, synovial fluid) Mus musculus 91-99 27597642-5 2016 We provide the first evidence for celastrol"s ability to inhibit the catalytic activity of sPLA2IIA, 5-LOX and COX-2 enzymes. celastrol 34-43 arachidonate 5-lipoxygenase Homo sapiens 101-106 27597642-5 2016 We provide the first evidence for celastrol"s ability to inhibit the catalytic activity of sPLA2IIA, 5-LOX and COX-2 enzymes. celastrol 34-43 prostaglandin-endoperoxide synthase 2 Homo sapiens 111-116 27597642-6 2016 Celastrol significantly inhibited the catalytic activity of sPLA2IIA (IC50=6muM) in vitro, which is independent of substrate and calcium concentration. celastrol 0-9 phospholipase A2, group IIA (platelets, synovial fluid) Mus musculus 60-68 27597642-7 2016 In addition, celastrol inhibited the catalytic activities of 5-LOX (IC50=5muM) and COX-2 (IC50=20muM) in vitro; sPLA2IIA-induced edema and carrageenan-induced edema in mice; and lipopolysaccharide-stimulated production of PGE2 in human neutrophils. celastrol 13-22 arachidonate 5-lipoxygenase Mus musculus 61-66 27597642-7 2016 In addition, celastrol inhibited the catalytic activities of 5-LOX (IC50=5muM) and COX-2 (IC50=20muM) in vitro; sPLA2IIA-induced edema and carrageenan-induced edema in mice; and lipopolysaccharide-stimulated production of PGE2 in human neutrophils. celastrol 13-22 prostaglandin-endoperoxide synthase 2 Homo sapiens 83-88 27597642-7 2016 In addition, celastrol inhibited the catalytic activities of 5-LOX (IC50=5muM) and COX-2 (IC50=20muM) in vitro; sPLA2IIA-induced edema and carrageenan-induced edema in mice; and lipopolysaccharide-stimulated production of PGE2 in human neutrophils. celastrol 13-22 phospholipase A2, group IIA (platelets, synovial fluid) Mus musculus 112-120 27768597-3 2016 This study investigates the impact of celastrol on the expression of death receptors 4/5 (DR4/5) on OS cell lines (HOS, U2OS) and cancer cell lysis by gammadelta T cells. celastrol 38-47 TNF receptor superfamily member 10a Homo sapiens 69-95 27768597-4 2016 The results showed that celastrol increased transcription of DR4/5 in HOS and U2OS, leading to increased cell surface, and total DR4/5 protein expression. celastrol 24-33 TNF receptor superfamily member 10a Homo sapiens 61-66 27768597-4 2016 The results showed that celastrol increased transcription of DR4/5 in HOS and U2OS, leading to increased cell surface, and total DR4/5 protein expression. celastrol 24-33 TNF receptor superfamily member 10a Homo sapiens 129-134 27768597-8 2016 Taken together, our data show that celastrol up-regulated DR4/5 on OS cells to be responsible for intercellular TRAIL/APO-2L crosslink that confers increased cancer cell lysis by gammadelta T cells. celastrol 35-44 TNF receptor superfamily member 10a Homo sapiens 58-63 27768597-8 2016 Taken together, our data show that celastrol up-regulated DR4/5 on OS cells to be responsible for intercellular TRAIL/APO-2L crosslink that confers increased cancer cell lysis by gammadelta T cells. celastrol 35-44 TNF superfamily member 10 Homo sapiens 112-124 27840916-0 2016 Effects of celastrol on enhancing apoptosis of ovarian cancer cells via the downregulation of microRNA-21 and the suppression of the PI3K/Akt-NF-kappaB signaling pathway in an in vitro model of ovarian carcinoma. celastrol 11-20 microRNA 21 Homo sapiens 94-105 27840916-0 2016 Effects of celastrol on enhancing apoptosis of ovarian cancer cells via the downregulation of microRNA-21 and the suppression of the PI3K/Akt-NF-kappaB signaling pathway in an in vitro model of ovarian carcinoma. celastrol 11-20 AKT serine/threonine kinase 1 Homo sapiens 138-141 27840916-5 2016 In OVCAR3 cells, celastrol was observed to suppress cellular proliferation, induce apoptosis and increase caspase-9 and -3 activity in a dose- and time-dependent manner. celastrol 17-26 caspase 9 Homo sapiens 106-122 27840916-6 2016 The expression levels of microRNA-21 (miRNA-21) were reduced, in addition to a reduction in the levels of phosphoinositide 3-kinase (PI3K)/p-Akt-NF (NF)-kappaB following treatment with celastrol. celastrol 185-194 microRNA 21 Homo sapiens 25-36 27840916-6 2016 The expression levels of microRNA-21 (miRNA-21) were reduced, in addition to a reduction in the levels of phosphoinositide 3-kinase (PI3K)/p-Akt-NF (NF)-kappaB following treatment with celastrol. celastrol 185-194 microRNA 21 Homo sapiens 38-46 27840916-7 2016 Notably, reduced expression of miRNA-21 replicated the effect of celastrol on OVCAR3 cells and inhibited the PI3K/p-Akt-NF-kappaB signaling pathway in an in vitro model of ovarian carcinoma. celastrol 65-74 microRNA 21 Homo sapiens 31-39 27840916-8 2016 To the best of our knowledge this is the first study to indicate that celastrol may represent a potential agent for the treatment of human ovarian carcinoma, via the induction of apoptosis through the downregulation of miRNA-21 and the PI3K/Akt-NF-kappaB signaling pathway in an in vitro model of ovarian carcinoma. celastrol 70-79 microRNA 21 Homo sapiens 219-227 27840916-8 2016 To the best of our knowledge this is the first study to indicate that celastrol may represent a potential agent for the treatment of human ovarian carcinoma, via the induction of apoptosis through the downregulation of miRNA-21 and the PI3K/Akt-NF-kappaB signaling pathway in an in vitro model of ovarian carcinoma. celastrol 70-79 AKT serine/threonine kinase 1 Homo sapiens 241-244 28123944-0 2017 Celastrol ameliorates liver metabolic damage caused by a high-fat diet through Sirt1. celastrol 0-9 sirtuin 1 Mus musculus 79-84 28123944-6 2017 RESULTS: When WT mice receiving a high-fat diet (HFD) were treated with Celastrol, reductions in body weight, subcutaneous and visceral fat content, and liver lipid droplet formation were observed, along with reduced hepatic intracellular triglyceride and serum triglyceride, free fatty acid, and ALT concentrations. celastrol 72-81 glutamic pyruvic transaminase, soluble Mus musculus 297-300 28123944-7 2017 Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase alpha (AMPKalpha), and increased the expression of hepatic serine-threonine liver kinase B1 (LKB1). celastrol 13-22 sterol regulatory element binding transcription factor 1 Mus musculus 41-85 28123944-7 2017 Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase alpha (AMPKalpha), and increased the expression of hepatic serine-threonine liver kinase B1 (LKB1). celastrol 13-22 sterol regulatory element binding transcription factor 1 Mus musculus 87-95 28123944-7 2017 Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase alpha (AMPKalpha), and increased the expression of hepatic serine-threonine liver kinase B1 (LKB1). celastrol 13-22 serine/threonine kinase 11 Mus musculus 254-269 28123944-7 2017 Furthermore, Celastrol decreased hepatic sterol regulatory element binding protein 1c (Srebp-1c) expression, enhanced the phosphorylation of hepatic AMP-activated protein kinase alpha (AMPKalpha), and increased the expression of hepatic serine-threonine liver kinase B1 (LKB1). celastrol 13-22 serine/threonine kinase 11 Mus musculus 271-275 28123944-9 2017 Celastrol administration also improved the anti-inflammatory and anti-oxidative status by inhibiting nuclear factor kappa B (NFkappaB) activity and the mRNA levels of proinflammatory cytokines and increasing mitochondrial DNA copy number and anti-oxidative stress genes expression in WT mice liver, in vivo and in vitro. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 101-123 28123944-9 2017 Celastrol administration also improved the anti-inflammatory and anti-oxidative status by inhibiting nuclear factor kappa B (NFkappaB) activity and the mRNA levels of proinflammatory cytokines and increasing mitochondrial DNA copy number and anti-oxidative stress genes expression in WT mice liver, in vivo and in vitro. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 125-133 28123944-10 2017 Moreover, Celastrol induced hepatic Sirt1 expression in WT mice, in vivo and in vitro. celastrol 10-19 sirtuin 1 Mus musculus 36-41 28123944-12 2017 It was more interesting that Celastrol aggravated HFD-induced liver damage in LKO mice fed a HFD by inhibiting the phosphorylation of AMPKalpha and boosting the translocation of NFkappaB into the nucleus, thereby resulting in the increase of Srebp-1c expression and the mRNA levels of liver proinflammatory cytokines. celastrol 29-38 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 178-186 28123944-12 2017 It was more interesting that Celastrol aggravated HFD-induced liver damage in LKO mice fed a HFD by inhibiting the phosphorylation of AMPKalpha and boosting the translocation of NFkappaB into the nucleus, thereby resulting in the increase of Srebp-1c expression and the mRNA levels of liver proinflammatory cytokines. celastrol 29-38 sterol regulatory element binding transcription factor 1 Mus musculus 242-250 28123944-14 2017 And Sirt1 has an important role in Celastrol-ameliorating liver metabolic damage caused by HFD. celastrol 35-44 sirtuin 1 Mus musculus 4-9 27658784-0 2016 The ROS derived mitochondrial respirstion not from NADPH oxidase plays key role in Celastrol against angiotensin II-mediated HepG2 cell proliferation. celastrol 83-92 angiotensinogen Homo sapiens 101-115 27658784-2 2016 Whether celastrol can effectively suppress AngII mediated cell proliferation remains unknown. celastrol 8-17 angiotensinogen Homo sapiens 43-48 27658784-3 2016 In this study, we studied the effect of celastrol on AngII-induced HepG2 cell proliferation and evaluated its underlying mechanism. celastrol 40-49 angiotensinogen Homo sapiens 53-58 27658784-7 2016 celastrol dramatically enhanced ROS generation, thereby causing cell apoptosis through inhibiting mitochodrial respiratory function and boosting the expression levels of AngII type 2 (AT2) receptor without influencing NADPH oxidase activity. celastrol 0-9 angiotensin II receptor type 2 Homo sapiens 170-182 27658784-7 2016 celastrol dramatically enhanced ROS generation, thereby causing cell apoptosis through inhibiting mitochodrial respiratory function and boosting the expression levels of AngII type 2 (AT2) receptor without influencing NADPH oxidase activity. celastrol 0-9 angiotensin II receptor type 2 Homo sapiens 184-187 27501757-0 2016 Downregulation of miR-17-92a cluster promotes autophagy induction in response to celastrol treatment in prostate cancer cells. celastrol 81-90 microRNA 17 Homo sapiens 18-24 27501757-3 2016 In the present study, we demonstrate that the miR-17-92a cluster plays a negative role in celastrol induced-autophagy. celastrol 90-99 microRNA 17 Homo sapiens 46-52 27501757-6 2016 Celastrol induced autophagy was inhibited by miR-20a or miR-17, while the inhibitory effects were rescued in the presence of pcDNA-ATG7 lacking 3" UTR, demonstrating that these two members target ATG7 to inhibit celastrol-induced autophagy. celastrol 0-9 microRNA 20a Homo sapiens 45-52 27501757-6 2016 Celastrol induced autophagy was inhibited by miR-20a or miR-17, while the inhibitory effects were rescued in the presence of pcDNA-ATG7 lacking 3" UTR, demonstrating that these two members target ATG7 to inhibit celastrol-induced autophagy. celastrol 0-9 microRNA 17 Homo sapiens 56-62 27501757-6 2016 Celastrol induced autophagy was inhibited by miR-20a or miR-17, while the inhibitory effects were rescued in the presence of pcDNA-ATG7 lacking 3" UTR, demonstrating that these two members target ATG7 to inhibit celastrol-induced autophagy. celastrol 0-9 autophagy related 7 Homo sapiens 131-135 27501757-6 2016 Celastrol induced autophagy was inhibited by miR-20a or miR-17, while the inhibitory effects were rescued in the presence of pcDNA-ATG7 lacking 3" UTR, demonstrating that these two members target ATG7 to inhibit celastrol-induced autophagy. celastrol 0-9 autophagy related 7 Homo sapiens 196-200 27501757-7 2016 As celastrol degrades androgen receptor (AR), a key transcription factor in prostate cancer cells, we further investigated whether AR affected miR-17-92a expression in prostate cancer cells. celastrol 3-12 androgen receptor Homo sapiens 22-39 27501757-7 2016 As celastrol degrades androgen receptor (AR), a key transcription factor in prostate cancer cells, we further investigated whether AR affected miR-17-92a expression in prostate cancer cells. celastrol 3-12 androgen receptor Homo sapiens 41-43 27501757-11 2016 In summary, our results demonstrate that celastrol downregulates AR and its target miR-17-92a, leading to autophagy induction in prostate cancer cells. celastrol 41-50 androgen receptor Homo sapiens 65-67 27501757-11 2016 In summary, our results demonstrate that celastrol downregulates AR and its target miR-17-92a, leading to autophagy induction in prostate cancer cells. celastrol 41-50 microRNA 17 Homo sapiens 83-89 27273088-7 2016 Celastrol activates heat shock transcription factor 1 (HSF1), the master regulator of Hsp gene transcription, and also exhibits potent anti-inflammatory and anti-oxidant activities. celastrol 0-9 heat shock transcription factor 1 Homo sapiens 55-59 27273088-7 2016 Celastrol activates heat shock transcription factor 1 (HSF1), the master regulator of Hsp gene transcription, and also exhibits potent anti-inflammatory and anti-oxidant activities. celastrol 0-9 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 86-89 27273088-10 2016 Co-application of celastrol and arimoclomol induced higher Hsp levels compared to heat shock paired with arimoclomol. celastrol 18-27 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 59-62 27496961-0 2016 Celastrol, a triterpene, enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and up-regulation of death receptors. celastrol 0-9 TNF superfamily member 10 Homo sapiens 34-39 27484716-0 2016 Celastrol inhibits IL-1beta-induced inflammation in orbital fibroblasts through the suppression of NF-kappaB activity. celastrol 0-9 interleukin 1 beta Homo sapiens 19-27 27484716-6 2016 Reverse transcription-polymerase chain reaction, western blotting and ELISAs were performed to examine the effect of celastrol on interleukin (IL)-1beta-induced inflammation in orbital fibroblasts from patients with GO. celastrol 117-126 interleukin 1 beta Homo sapiens 130-152 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 interleukin 6 Homo sapiens 83-87 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 C-X-C motif chemokine ligand 8 Homo sapiens 89-93 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 mitochondrially encoded cytochrome c oxidase II Homo sapiens 95-117 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 intercellular adhesion molecule 1 Homo sapiens 122-155 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 intercellular adhesion molecule 1 Homo sapiens 157-163 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 interleukin 1 beta Homo sapiens 180-188 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 interleukin 6 Homo sapiens 228-232 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 C-X-C motif chemokine ligand 8 Homo sapiens 234-238 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 intercellular adhesion molecule 1 Homo sapiens 240-246 27484716-7 2016 The results demonstrated that celastrol significantly attenuated the expression of IL-6, IL-8, cyclooxygenase (COX)-2 and intercellular adhesion molecule-1 (ICAM-1), and inhibited IL-1beta-induced increases in the expression of IL-6, IL-8, ICAM-1 and COX-2. celastrol 30-39 mitochondrially encoded cytochrome c oxidase II Homo sapiens 251-256 27484716-8 2016 The levels of prostaglandin E2 in orbital fibroblasts induced by IL-1beta were also suppressed by celastrol. celastrol 98-107 interleukin 1 beta Homo sapiens 65-73 27484716-9 2016 Further investigation revealed that celastrol suppressed the IL-1beta-induced inflammatory responses in orbital fibroblasts through inhibiting the activation of nuclear factor (NF)-kappaB. celastrol 36-45 interleukin 1 beta Homo sapiens 61-69 27484716-9 2016 Further investigation revealed that celastrol suppressed the IL-1beta-induced inflammatory responses in orbital fibroblasts through inhibiting the activation of nuclear factor (NF)-kappaB. celastrol 36-45 nuclear factor kappa B subunit 1 Homo sapiens 161-187 27484716-10 2016 Taken together, these results suggested that celastrol attenuated the IL-1beta-induced pro-inflammatory pathway in orbital fibroblasts from patients with GO, which was associated with the suppression of NF-kappaB activation. celastrol 45-54 interleukin 1 beta Homo sapiens 70-78 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 135-138 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 BCL2, apoptosis regulator Rattus norvegicus 165-170 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 Bcl2-like 1 Rattus norvegicus 175-181 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 BCL2 associated X, apoptosis regulator Rattus norvegicus 209-212 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 poly (ADP-ribose) polymerase family, member 1 Mus musculus 228-232 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 caspase 9 Mus musculus 237-245 27425825-7 2016 A small chemical library composed of synthetic compounds and natural extracts were screened with the method, two natural products, namely, demethylzeylasteral and celastrol, were identified as new inhibitors to block the Bcl-XL-Bid interaction. celastrol 163-172 BCL2 like 1 Homo sapiens 221-227 27425825-7 2016 A small chemical library composed of synthetic compounds and natural extracts were screened with the method, two natural products, namely, demethylzeylasteral and celastrol, were identified as new inhibitors to block the Bcl-XL-Bid interaction. celastrol 163-172 BH3 interacting domain death agonist Homo sapiens 228-231 27181068-8 2016 Moreover, Celastrol obviously improved the hepatic pathological lesions and decreased the elevated levels of ALT, AST, ALP and AFP. celastrol 10-19 glutamic pyruvic transaminase, soluble Mus musculus 109-112 27181068-8 2016 Moreover, Celastrol obviously improved the hepatic pathological lesions and decreased the elevated levels of ALT, AST, ALP and AFP. celastrol 10-19 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 114-117 27181068-8 2016 Moreover, Celastrol obviously improved the hepatic pathological lesions and decreased the elevated levels of ALT, AST, ALP and AFP. celastrol 10-19 alpha-fetoprotein Rattus norvegicus 127-130 27181068-9 2016 Meanwhile, Celastrol suppressed the expression of the protein MDM2, activated the intrinsic mitochondrial apoptosis pathway induced by p53, inhibited anti-apoptotic Bcl-2 and Bcl-xl, induced the pro-apoptotic Bax, cytochrome C, PARP and caspases. celastrol 11-20 MDM2 proto-oncogene Rattus norvegicus 62-66 26842874-5 2016 Notably, several food compounds, such as teasaponins, resveratrol, celastrol, caffeine, and taurine among others, are able to restore the leptin signaling in neurons by overexpressing anorexigenic peptides (proopiomelanocortin) and/or repressing orexigenic peptides (neuropeptide Y/agouti-related peptide), thus decreasing food intake. celastrol 67-76 leptin Homo sapiens 138-144 27235383-1 2016 Celastrol (CEL), a plant-derived triterpenoid, is a known inhibitor of Hsp90 and NF-kappaB activation pathways and has recently been suggested to be of therapeutic importance in various cancers. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 71-76 27235383-1 2016 Celastrol (CEL), a plant-derived triterpenoid, is a known inhibitor of Hsp90 and NF-kappaB activation pathways and has recently been suggested to be of therapeutic importance in various cancers. celastrol 11-14 heat shock protein 90 alpha family class A member 1 Homo sapiens 71-76 27159672-11 2016 The results indicated that celastrol is a substrate of P-glycoprotein but not multidrug resistance protein 2 or the breast cancer resistance protein. celastrol 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 55-69 27159672-8 2016 Additionally, the effects of celastrol on the activity of P-glycoprotein were evaluated using the rhodamine 123 uptake assay. celastrol 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 27405485-5 2016 Identification of the molecular targets of celastrol such as the NF-kappaB pathway, MAPK pathway, JAK/STAT pathway and RANKL/OPG pathway has unraveled its strategic checkpoints in controlling arthritic inflammation and tissue damage in AA. celastrol 43-52 basic transcription factor 3 pseudogene 11 Homo sapiens 125-128 27374097-4 2016 Firstly, multiple assays indicated that celastrol could induce apoptosis of APL cells via p53-activated mitochondrial pathway. celastrol 40-49 tumor protein p53 Homo sapiens 90-93 27374097-9 2016 Celastrol could also decrease uridine and DHODH protein level in tumor tissues. celastrol 0-9 dihydroorotate dehydrogenase (quinone) Homo sapiens 42-47 27017606-12 2016 An in vitro isotope tracing experiment showed that COT and its bioactive ingredients, such as celastrol, ursolic acid, oleanolic acid, and quercetin, significantly increased the efflux of (3)H-cholesterol. celastrol 94-103 mitogen-activated protein kinase kinase kinase 8 Mus musculus 51-54 27049825-0 2016 Celastrol attenuates oxidative stress in the skeletal muscle of diabetic rats by regulating the AMPK-PGC1alpha-SIRT3 signaling pathway. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 96-100 27398312-0 2016 Mutations Y493G and K546D in human HSP90 disrupt binding of celastrol and reduce interaction with Cdc37. celastrol 60-69 heat shock protein 90 alpha family class A member 1 Homo sapiens 35-40 27398312-1 2016 Celastrol, a natural compound derived from the Chinese herb Tripterygium wilfordii Hook F, has been proven to inhibit heat shock protein 90 (HSP90) activity and has attracted much attention because of its promising effects in cancer treatment and in ameliorating degenerative neuron diseases. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 141-146 27398312-2 2016 However, the HSP90 structure involved in celastrol interaction is not known. celastrol 41-50 heat shock protein 90 alpha family class A member 1 Homo sapiens 13-18 27398312-3 2016 Here, we report a novel celastrol-binding pocket in the HSP90 dimer, predicted by molecular docking. celastrol 24-33 heat shock protein 90 alpha family class A member 1 Homo sapiens 56-61 27398312-4 2016 Mutation of the two key binding pocket amino acids (Lys546 and Tyr493) disrupted the binding of celastrol to HSP90 dimers, as detected by isothermal titration calorimetry (ITC). celastrol 96-105 heat shock protein 90 alpha family class A member 1 Homo sapiens 109-114 27398312-5 2016 Interestingly, such mutations also reduced binding between HSP90 and the cochaperone Cdc37, thus providing a new explanation for reported findings that celastrol shows more obvious effects in disrupting binding between HSP90 and Cdc37 than between HSP90 and other cochaperones. celastrol 152-161 heat shock protein 90 alpha family class A member 1 Homo sapiens 59-64 27398312-5 2016 Interestingly, such mutations also reduced binding between HSP90 and the cochaperone Cdc37, thus providing a new explanation for reported findings that celastrol shows more obvious effects in disrupting binding between HSP90 and Cdc37 than between HSP90 and other cochaperones. celastrol 152-161 cell division cycle 37, HSP90 cochaperone Homo sapiens 85-90 27398312-5 2016 Interestingly, such mutations also reduced binding between HSP90 and the cochaperone Cdc37, thus providing a new explanation for reported findings that celastrol shows more obvious effects in disrupting binding between HSP90 and Cdc37 than between HSP90 and other cochaperones. celastrol 152-161 heat shock protein 90 alpha family class A member 1 Homo sapiens 219-224 27398312-5 2016 Interestingly, such mutations also reduced binding between HSP90 and the cochaperone Cdc37, thus providing a new explanation for reported findings that celastrol shows more obvious effects in disrupting binding between HSP90 and Cdc37 than between HSP90 and other cochaperones. celastrol 152-161 cell division cycle 37, HSP90 cochaperone Homo sapiens 229-234 27398312-5 2016 Interestingly, such mutations also reduced binding between HSP90 and the cochaperone Cdc37, thus providing a new explanation for reported findings that celastrol shows more obvious effects in disrupting binding between HSP90 and Cdc37 than between HSP90 and other cochaperones. celastrol 152-161 heat shock protein 90 alpha family class A member 1 Homo sapiens 219-224 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 71-80 heat shock protein 90 alpha family class A member 1 Homo sapiens 55-60 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 71-80 heat shock protein 90 alpha family class A member 1 Homo sapiens 152-157 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 71-80 cell division cycle 37, HSP90 cochaperone Homo sapiens 162-167 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 119-128 heat shock protein 90 alpha family class A member 1 Homo sapiens 55-60 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 119-128 heat shock protein 90 alpha family class A member 1 Homo sapiens 152-157 27398312-6 2016 In short, our work discloses a novel binding pocket in HSP90 dimer for celastrol and provides an explanation as to why celastrol has a strong effect on HSP90 and Cdc37 binding. celastrol 119-128 cell division cycle 37, HSP90 cochaperone Homo sapiens 162-167 27049825-0 2016 Celastrol attenuates oxidative stress in the skeletal muscle of diabetic rats by regulating the AMPK-PGC1alpha-SIRT3 signaling pathway. celastrol 0-9 PPARG coactivator 1 alpha Rattus norvegicus 101-110 27049825-0 2016 Celastrol attenuates oxidative stress in the skeletal muscle of diabetic rats by regulating the AMPK-PGC1alpha-SIRT3 signaling pathway. celastrol 0-9 sirtuin 3 Rattus norvegicus 111-116 27049825-11 2016 Celastrol exerted antioxidant effects on skeletal muscle partly by regulating the AMPK-PGC1alpha-Sirt3 signaling pathway. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 82-86 27049825-11 2016 Celastrol exerted antioxidant effects on skeletal muscle partly by regulating the AMPK-PGC1alpha-Sirt3 signaling pathway. celastrol 0-9 PPARG coactivator 1 alpha Rattus norvegicus 87-96 27049825-11 2016 Celastrol exerted antioxidant effects on skeletal muscle partly by regulating the AMPK-PGC1alpha-Sirt3 signaling pathway. celastrol 0-9 sirtuin 3 Homo sapiens 97-102 27110686-6 2016 In addition, we show that short-term in vivo treatment with low dosages of two molecularly distinct proteasome inhibitors celastrol and epoxomicin reverse hyperglycemia in mice with beta-cell failure by increasing insulin production and insulin sensitivity. celastrol 122-131 insulin Homo sapiens 214-221 27085773-0 2016 Cascade regulation of PPARgamma(2) and C/EBPalpha signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes. celastrol 72-81 peroxisome proliferator activated receptor gamma Mus musculus 22-34 27085773-0 2016 Cascade regulation of PPARgamma(2) and C/EBPalpha signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes. celastrol 72-81 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 39-49 27085773-6 2016 RESULTS: Treatment of celastrol not only inhibited adipocyte differentiation (lipid accumulation, glyceraldehyde-3-phosphate dehydrogenase activity and triglyceride content) but also increased lipolysis (glycerol release and free fatty acid release) in 3T3-L1 adipocytes. celastrol 22-31 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 98-138 27085773-7 2016 In addition, all celastrol-regulated functional activities were controlled by PPARgamma(2) and C/EBPalpha signaling pathways in duration of celastrol"s treatment in 3T3-L1 adipocytes. celastrol 17-26 peroxisome proliferator activated receptor gamma Mus musculus 78-90 27085773-7 2016 In addition, all celastrol-regulated functional activities were controlled by PPARgamma(2) and C/EBPalpha signaling pathways in duration of celastrol"s treatment in 3T3-L1 adipocytes. celastrol 17-26 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 95-105 27085773-7 2016 In addition, all celastrol-regulated functional activities were controlled by PPARgamma(2) and C/EBPalpha signaling pathways in duration of celastrol"s treatment in 3T3-L1 adipocytes. celastrol 140-149 peroxisome proliferator activated receptor gamma Mus musculus 78-90 27085773-7 2016 In addition, all celastrol-regulated functional activities were controlled by PPARgamma(2) and C/EBPalpha signaling pathways in duration of celastrol"s treatment in 3T3-L1 adipocytes. celastrol 140-149 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 95-105 27085773-8 2016 CONCLUSION: Our initial data from in vitro celastrol signaling studies suggest novel insights into the role of PPARgamma(2) and C/EBPalpha as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes. celastrol 178-187 peroxisome proliferator activated receptor gamma Mus musculus 111-123 27085773-8 2016 CONCLUSION: Our initial data from in vitro celastrol signaling studies suggest novel insights into the role of PPARgamma(2) and C/EBPalpha as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes. celastrol 178-187 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 128-138 27144550-0 2016 Celastrol Induces Cell Apoptosis and Inhibits the Expression of the AML1-ETO/C-KIT Oncoprotein in t(8;21) Leukemia. celastrol 0-9 RUNX family transcription factor 1 Homo sapiens 68-72 27144550-0 2016 Celastrol Induces Cell Apoptosis and Inhibits the Expression of the AML1-ETO/C-KIT Oncoprotein in t(8;21) Leukemia. celastrol 0-9 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 73-76 27144550-0 2016 Celastrol Induces Cell Apoptosis and Inhibits the Expression of the AML1-ETO/C-KIT Oncoprotein in t(8;21) Leukemia. celastrol 0-9 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 77-82 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 RUNX family transcription factor 1 Homo sapiens 55-59 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 60-63 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 105-110 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 AKT serine/threonine kinase 1 Homo sapiens 134-137 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 signal transducer and activator of transcription 3 Homo sapiens 139-144 27144550-6 2016 In addition, we found that celastrol downregulated the AML1-ETO fusion protein, therefore downregulating C-KIT kinases and inhibiting AKT, STAT3 and Erk1/2. celastrol 27-36 mitogen-activated protein kinase 3 Homo sapiens 149-155 27181127-6 2016 RESULTS: The results showed that celastrol could effectively inhibit PA-caused TLR4-dependent NF-kappaB activation in the HepG2 cells; PA also activated IRAKs, which were inhibited by celastrol. celastrol 33-42 toll like receptor 4 Homo sapiens 79-83 27021137-3 2016 Celastrol treatment significantly alleviated DSS-induced colitis in mice, as revealed by the body weight, colon length, scores of rectal bleeding and diarrhea, serum TNF-alpha level, and histological analysis results. celastrol 0-9 tumor necrosis factor Mus musculus 166-175 27021137-7 2016 Quantitative real-time PCR analysis revealed that the liver expression of stearoyl-coenzyme A desaturase 1 (SCD1), the key enzyme controlling the desaturation of saturated fatty acid, was dramatically inhibited in IBD mice, and was obviously recovered after celastrol treatment. celastrol 258-267 stearoyl-Coenzyme A desaturase 1 Mus musculus 74-106 27021137-7 2016 Quantitative real-time PCR analysis revealed that the liver expression of stearoyl-coenzyme A desaturase 1 (SCD1), the key enzyme controlling the desaturation of saturated fatty acid, was dramatically inhibited in IBD mice, and was obviously recovered after celastrol treatment. celastrol 258-267 stearoyl-Coenzyme A desaturase 1 Mus musculus 108-112 27021137-8 2016 These results suggest that the increased saturated LPC/unsaturated LPC (and saturated fatty acid/unsaturated fatty acid) ratios associated with SCD1 down-regulation could be regarded as biomarkers of colitis, and celastrol alleviates DSS-induced colitis partially via up-regulation of SCD1, restoring the altered balance between stearic acid- and oleic acid-derived lipid species, which plays an important role in alleviating colitis. celastrol 213-222 stearoyl-Coenzyme A desaturase 1 Mus musculus 285-289 27110686-6 2016 In addition, we show that short-term in vivo treatment with low dosages of two molecularly distinct proteasome inhibitors celastrol and epoxomicin reverse hyperglycemia in mice with beta-cell failure by increasing insulin production and insulin sensitivity. celastrol 122-131 insulin Homo sapiens 237-244 26631113-4 2016 We have identified the triterpenoid Celastrol as a potent low-molecular-weight inhibitor of the interaction of Myb with its cooperation partner p300. celastrol 36-45 MYB proto-oncogene, transcription factor Homo sapiens 111-114 26980429-0 2016 Celastrol, an NF-kappaB inhibitor, ameliorates hypercalciuria and articular cartilage lesions in a mouse model of secondary osteoporosis. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 14-23 26980429-2 2016 In this study, therefore, we evaluated the role of celastrol, an NF-kappaB inhibitor, in a mouse model of secondary osteoporosis. celastrol 51-60 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 65-74 26980429-6 2016 Moreover, other important events were observed after celastrol treatment, covering substantial decrements in serum concentrations of PTH, TRAP-5b, CTX and DPD, improved structure of articular cartilage and cancellous bone (revealed by H&E and safranin-O staining), and significant decline in levels of NF-kappaB (P65), MMP-1, and MMP-9. celastrol 53-62 parathyroid hormone Mus musculus 133-136 26980429-6 2016 Moreover, other important events were observed after celastrol treatment, covering substantial decrements in serum concentrations of PTH, TRAP-5b, CTX and DPD, improved structure of articular cartilage and cancellous bone (revealed by H&E and safranin-O staining), and significant decline in levels of NF-kappaB (P65), MMP-1, and MMP-9. celastrol 53-62 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 306-315 26980429-6 2016 Moreover, other important events were observed after celastrol treatment, covering substantial decrements in serum concentrations of PTH, TRAP-5b, CTX and DPD, improved structure of articular cartilage and cancellous bone (revealed by H&E and safranin-O staining), and significant decline in levels of NF-kappaB (P65), MMP-1, and MMP-9. celastrol 53-62 matrix metallopeptidase 13 Mus musculus 323-328 26980429-6 2016 Moreover, other important events were observed after celastrol treatment, covering substantial decrements in serum concentrations of PTH, TRAP-5b, CTX and DPD, improved structure of articular cartilage and cancellous bone (revealed by H&E and safranin-O staining), and significant decline in levels of NF-kappaB (P65), MMP-1, and MMP-9. celastrol 53-62 matrix metallopeptidase 9 Mus musculus 334-339 26631113-4 2016 We have identified the triterpenoid Celastrol as a potent low-molecular-weight inhibitor of the interaction of Myb with its cooperation partner p300. celastrol 36-45 E1A binding protein p300 Homo sapiens 144-148 26793111-6 2015 Mechanically, celastrol treatment significantly prevented AOM/DSS-induced up-regulation of expression levels of oncologic markers including mutated p53 and phospho-p53, beta-catenin and proliferating cell nuclear antigen (PCNA). celastrol 14-23 transformation related protein 53, pseudogene Mus musculus 148-151 26768587-0 2016 Celastrol enhances Nrf2 mediated antioxidant enzymes and exhibits anti-fibrotic effect through regulation of collagen production against bleomycin-induced pulmonary fibrosis. celastrol 0-9 NFE2 like bZIP transcription factor 2 Rattus norvegicus 19-23 26768587-8 2016 Celastrol also reduces inflammation in BLM-induced rats as evidenced by decrease in the expressions of mast cells, Tumor necrosis factor-alpha (TNF- alpha) and matrix metalloproteinases (MMPs) 2 and 9. celastrol 0-9 tumor necrosis factor Rattus norvegicus 115-142 26768587-8 2016 Celastrol also reduces inflammation in BLM-induced rats as evidenced by decrease in the expressions of mast cells, Tumor necrosis factor-alpha (TNF- alpha) and matrix metalloproteinases (MMPs) 2 and 9. celastrol 0-9 tumor necrosis factor Rattus norvegicus 144-154 26768587-9 2016 Further, Western blot analysis shows that celastrol is a potent inducer of NF-E2-related factor 2 (Nrf2) and it restores the activities of Phase II enzymes such as hemoxygenase-1 (HO-1), glutathione-S-transferase (GSTs) and NADP(H): quinine oxidoreductase (NQO1) which were declined upon BLM administration. celastrol 42-51 NFE2 like bZIP transcription factor 2 Rattus norvegicus 99-103 26793111-6 2015 Mechanically, celastrol treatment significantly prevented AOM/DSS-induced up-regulation of expression levels of oncologic markers including mutated p53 and phospho-p53, beta-catenin and proliferating cell nuclear antigen (PCNA). celastrol 14-23 transformation related protein 53, pseudogene Mus musculus 164-167 26793111-6 2015 Mechanically, celastrol treatment significantly prevented AOM/DSS-induced up-regulation of expression levels of oncologic markers including mutated p53 and phospho-p53, beta-catenin and proliferating cell nuclear antigen (PCNA). celastrol 14-23 catenin (cadherin associated protein), beta 1 Mus musculus 169-181 26793111-6 2015 Mechanically, celastrol treatment significantly prevented AOM/DSS-induced up-regulation of expression levels of oncologic markers including mutated p53 and phospho-p53, beta-catenin and proliferating cell nuclear antigen (PCNA). celastrol 14-23 proliferating cell nuclear antigen Mus musculus 186-220 26793111-6 2015 Mechanically, celastrol treatment significantly prevented AOM/DSS-induced up-regulation of expression levels of oncologic markers including mutated p53 and phospho-p53, beta-catenin and proliferating cell nuclear antigen (PCNA). celastrol 14-23 proliferating cell nuclear antigen Mus musculus 222-226 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 tumor necrosis factor Mus musculus 110-137 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 tumor necrosis factor Mus musculus 139-148 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 interleukin 1 beta Mus musculus 151-173 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 interleukin 6 Mus musculus 178-182 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 prostaglandin-endoperoxide synthase 2 Mus musculus 203-219 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 prostaglandin-endoperoxide synthase 2 Mus musculus 221-226 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 nitric oxide synthase 2, inducible Mus musculus 232-263 26793111-7 2015 In addition, treatment with celastrol inhibited inflammatory responses, as indicated by the decrease of serum tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta and IL-6, down-regulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), and inactivation of nuclear factor kappaB (NF-kappaB). celastrol 28-37 nitric oxide synthase 2, inducible Mus musculus 265-269 26793111-8 2015 Moreover, celastrol obviously suppressed epithelial-mesenchymal transition (EMT) through up-regulating E-cadherin and down-regulating N-cadherin, Vimentin and Snail. celastrol 10-19 cadherin 1 Mus musculus 103-113 26793111-8 2015 Moreover, celastrol obviously suppressed epithelial-mesenchymal transition (EMT) through up-regulating E-cadherin and down-regulating N-cadherin, Vimentin and Snail. celastrol 10-19 cadherin 2 Mus musculus 134-144 26793111-8 2015 Moreover, celastrol obviously suppressed epithelial-mesenchymal transition (EMT) through up-regulating E-cadherin and down-regulating N-cadherin, Vimentin and Snail. celastrol 10-19 vimentin Mus musculus 146-154 26793111-8 2015 Moreover, celastrol obviously suppressed epithelial-mesenchymal transition (EMT) through up-regulating E-cadherin and down-regulating N-cadherin, Vimentin and Snail. celastrol 10-19 snail family zinc finger 1 Mus musculus 159-164 27160852-0 2016 Celastrol-Induced Suppression of the MiR-21/ERK Signalling Pathway Attenuates Cardiac Fibrosis and Dysfunction. celastrol 0-9 microRNA 21a Mus musculus 37-43 27671821-5 2016 The major cell signaling pathways modulated by celastrol include the NF-kB pathway, MAPK pathway, JAK/STAT pathway, PI3K/Akt/mTOR pathway, and antioxidant defense mechanisms. celastrol 47-56 AKT serine/threonine kinase 1 Homo sapiens 121-124 27671821-5 2016 The major cell signaling pathways modulated by celastrol include the NF-kB pathway, MAPK pathway, JAK/STAT pathway, PI3K/Akt/mTOR pathway, and antioxidant defense mechanisms. celastrol 47-56 mechanistic target of rapamycin kinase Homo sapiens 125-129 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 myosin, heavy polypeptide 7, cardiac muscle, beta Mus musculus 222-230 26760966-9 2016 Celastrol therapy inhibited Hsp90 mRNA and protein levels and up-regulated the expressions of receptor Flk-1 in TD-affected tibial growth plates significantly (P < 0.05) in addition to rectifying the damaging effects of thiram on the liver by decreasing the levels of aspartate aminotransferase, alanine aminotransferase and malondialdehyde and correcting the oxidative imbalance. celastrol 0-9 kinase insert domain receptor Gallus gallus 103-108 27160852-0 2016 Celastrol-Induced Suppression of the MiR-21/ERK Signalling Pathway Attenuates Cardiac Fibrosis and Dysfunction. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 44-47 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 microRNA 21a Mus musculus 233-239 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 actin alpha 2, smooth muscle, aorta Mus musculus 90-115 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 244-249 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 mitogen-activated protein kinase 1 Mus musculus 246-249 27160852-13 2016 Celastrol treatment reduced myocardial fibroblast viability and collagen content and down-regulated alpha-SMA in cultured CFs in vitro. celastrol 0-9 actin alpha 2, smooth muscle, aorta Mus musculus 100-109 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 actin alpha 2, smooth muscle, aorta Mus musculus 117-126 27160852-14 2016 Celastrol also inhibited the miR-21/ERK signalling pathway. celastrol 0-9 microRNA 21a Mus musculus 29-35 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 natriuretic peptide type A Mus musculus 129-155 27160852-14 2016 Celastrol also inhibited the miR-21/ERK signalling pathway. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 36-39 27160852-15 2016 Celastrol attenuated miR-21 up-regulation by TGF-beta1 and decreased elevated p-ERK/ERK levels in CFs transfected with miR-21. celastrol 0-9 microRNA 21a Mus musculus 21-27 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 natriuretic peptide type B Mus musculus 191-194 27160852-15 2016 Celastrol attenuated miR-21 up-regulation by TGF-beta1 and decreased elevated p-ERK/ERK levels in CFs transfected with miR-21. celastrol 0-9 transforming growth factor, beta 1 Mus musculus 45-54 27160852-15 2016 Celastrol attenuated miR-21 up-regulation by TGF-beta1 and decreased elevated p-ERK/ERK levels in CFs transfected with miR-21. celastrol 0-9 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 78-83 27160852-15 2016 Celastrol attenuated miR-21 up-regulation by TGF-beta1 and decreased elevated p-ERK/ERK levels in CFs transfected with miR-21. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 80-83 27160852-11 2016 RESULTS: Celastrol treatment reduced the increased collagen deposition and down-regulated alpha-smooth muscle actin (alpha-SMA), atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP), beta-myosin heavy chain (beta-MHC), miR-21 and p-ERK/ERK. celastrol 9-18 myosin, heavy polypeptide 7, cardiac muscle, beta Mus musculus 197-220 27160852-15 2016 Celastrol attenuated miR-21 up-regulation by TGF-beta1 and decreased elevated p-ERK/ERK levels in CFs transfected with miR-21. celastrol 0-9 microRNA 21a Mus musculus 119-125 27160852-17 2016 Celastrol ameliorates myocardial fibrosis and cardiac dysfunction, these probably related to miR-21/ERK signaling pathways in vitro and in vivo. celastrol 0-9 microRNA 21a Mus musculus 93-99 27057550-0 2016 Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-kappaB Signaling Pathway in Type 2 Diabetic Rats. celastrol 22-31 toll-like receptor 4 Rattus norvegicus 61-65 27160852-17 2016 Celastrol ameliorates myocardial fibrosis and cardiac dysfunction, these probably related to miR-21/ERK signaling pathways in vitro and in vivo. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 100-103 27072230-1 2016 AIM OF STUDY: Embelin and celastrol, inhibitors of XIAP and NF-kappaB proteins respectively, have been derived from natural sources and shown anti-tumor activities against different cancer cell lines. celastrol 26-35 X-linked inhibitor of apoptosis Homo sapiens 51-55 27072230-12 2016 Therefore targeting XIAP and NF-kappaB pathways simultaneously can be investigated in more detail to make use of embelin and celastrol as a combination therapy of cancer. celastrol 125-134 X-linked inhibitor of apoptosis Homo sapiens 20-24 27057550-0 2016 Protective Effects of Celastrol on Diabetic Liver Injury via TLR4/MyD88/NF-kappaB Signaling Pathway in Type 2 Diabetic Rats. celastrol 22-31 MYD88, innate immune signal transduction adaptor Rattus norvegicus 66-71 27057550-9 2016 We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-kappaB signaling cascade pathways and its downstream inflammatory effectors. celastrol 22-31 toll-like receptor 4 Rattus norvegicus 138-142 27057550-9 2016 We firstly found that celastrol treatment could delay the progression of diabetic liver disease in type 2 diabetic rats via inhibition of TLR4/MyD88/NF-kappaB signaling cascade pathways and its downstream inflammatory effectors. celastrol 22-31 MYD88, innate immune signal transduction adaptor Rattus norvegicus 143-148 26658436-0 2015 Decrease of CD68 Synovial Macrophages in Celastrol Treated Arthritic Rats. celastrol 41-50 Cd68 molecule Rattus norvegicus 12-16 26658436-4 2015 We have shown, in vitro, that celastrol inhibits both IL-1beta and TNF, which play an important role in RA, and, in vivo, that celastrol has significant anti-inflammatory properties. celastrol 30-39 interleukin 1 beta Rattus norvegicus 54-62 26658436-4 2015 We have shown, in vitro, that celastrol inhibits both IL-1beta and TNF, which play an important role in RA, and, in vivo, that celastrol has significant anti-inflammatory properties. celastrol 30-39 tumor necrosis factor Rattus norvegicus 67-70 26658436-5 2015 Our main goal in this work was to test the effect of celastrol in the number of sublining CD68 macrophages (a biomarker of therapeutic response for novel RA treatments) and on the overall synovial tissue cellularity and joint structure in the adjuvant-induced rat model of arthritis (AIA). celastrol 53-62 Cd68 molecule Rattus norvegicus 90-94 26658436-9 2015 RESULTS: Here we report that celastrol significantly decreases the number of sublining CD68 macrophages and the overall synovial inflammatory cellularity, and halted joint destruction without side effects. celastrol 29-38 Cd68 molecule Rattus norvegicus 87-91 26510321-0 2015 Targeting Mast Cells and Basophils with Anti-FcepsilonRIalpha Fab-Conjugated Celastrol-Loaded Micelles Suppresses Allergic Inflammation. celastrol 77-86 FA complementation group B Homo sapiens 62-65 26454701-8 2015 Our results showed that celastrol treatment ameliorated the severity of colitis, decreased the level of interleukin (IL)-1beta, IL-6 and myeloperoxidase (MPO) and upregulated the level of E-cadherin in colitis mice. celastrol 24-33 myeloperoxidase Mus musculus 137-152 26454701-8 2015 Our results showed that celastrol treatment ameliorated the severity of colitis, decreased the level of interleukin (IL)-1beta, IL-6 and myeloperoxidase (MPO) and upregulated the level of E-cadherin in colitis mice. celastrol 24-33 myeloperoxidase Mus musculus 154-157 26454701-8 2015 Our results showed that celastrol treatment ameliorated the severity of colitis, decreased the level of interleukin (IL)-1beta, IL-6 and myeloperoxidase (MPO) and upregulated the level of E-cadherin in colitis mice. celastrol 24-33 cadherin 1 Mus musculus 188-198 26454701-10 2015 On the mechanism, decreased level of necroptosis factors RIP3 and MLKL, and increased level of active caspase-8 were detected after celastrol treatment. celastrol 132-141 receptor-interacting serine-threonine kinase 3 Mus musculus 57-61 26454701-10 2015 On the mechanism, decreased level of necroptosis factors RIP3 and MLKL, and increased level of active caspase-8 were detected after celastrol treatment. celastrol 132-141 mixed lineage kinase domain-like Mus musculus 66-70 26454701-10 2015 On the mechanism, decreased level of necroptosis factors RIP3 and MLKL, and increased level of active caspase-8 were detected after celastrol treatment. celastrol 132-141 caspase 8 Mus musculus 102-111 26454701-11 2015 Taken together, our results demonstrated that celastrol exerted beneficial effects in colitis treatment via suppressing the RIP3/MLKL necroptosis pathway. celastrol 46-55 receptor-interacting serine-threonine kinase 3 Mus musculus 124-128 26454701-11 2015 Taken together, our results demonstrated that celastrol exerted beneficial effects in colitis treatment via suppressing the RIP3/MLKL necroptosis pathway. celastrol 46-55 mixed lineage kinase domain-like Mus musculus 129-133 26510321-3 2015 Our present study aims at targeted delivery of anti-FcepsilonRIalpha Fab-conjugated celastrol-loaded micelles toward FcepsilonRIalpha receptors expressed on mast cells and basophils to have enhanced anti-allergic effect. celastrol 84-93 FA complementation group B Homo sapiens 69-72 26510321-6 2015 The anti-FcepsilonRIalpha Fab-conjugated celastrol-loaded micelles revealed uniform particle size (93.43 +- 12.93 nm) with high loading percentage (21.2 +- 1.5% w/w). celastrol 41-50 FA complementation group B Homo sapiens 26-29 26510321-11 2015 In addition, in mouse model of passive cutaneous anaphylaxis, anti-FcepsilonRIalpha Fab-conjugated celastrol-loaded micelles treatment significantly decreased extravasated evan"s in the ear. celastrol 99-108 FA complementation group B Homo sapiens 84-87 26510321-12 2015 These results indicate that anti-FcepsilonRIalpha Fab-conjugated celastrol-loaded micelles can target and selectively kill mast cells and basophils which express FcepsilonRIalpha, and may be efficient reagents for the treatment of allergic disorders and mast cell related diseases. celastrol 65-74 FA complementation group B Homo sapiens 50-53 26552919-0 2015 Inhibiting inducible miR-223 further reduces viable cells in human cancer cell lines MCF-7 and PC3 treated by celastrol. celastrol 110-119 microRNA 223 Homo sapiens 21-28 26552919-0 2015 Inhibiting inducible miR-223 further reduces viable cells in human cancer cell lines MCF-7 and PC3 treated by celastrol. celastrol 110-119 chromobox 8 Homo sapiens 95-98 26552919-3 2015 METHODS AND RESULTS: Here, we report that celastrol treatment can elevate miR-223 in human breast cancer cell line MCF-7 and prostate cancer PC3. celastrol 42-51 microRNA 223 Homo sapiens 74-81 26552919-3 2015 METHODS AND RESULTS: Here, we report that celastrol treatment can elevate miR-223 in human breast cancer cell line MCF-7 and prostate cancer PC3. celastrol 42-51 chromobox 8 Homo sapiens 141-144 26552919-4 2015 Down-regulating miR-223 could increase the number of viable cells, yet it further reduced viable cells in samples that were treated by celastrol; up-regulation of miR-223 displayed opposite effects. celastrol 135-144 microRNA 223 Homo sapiens 16-23 26552919-5 2015 Celastrol"s miR-223 induction might be due to NF-kappaB inhibition and transient mTOR activation: these two events occurred prior to miR-223 elevation in celastrol-treated cells. celastrol 0-9 microRNA 223 Homo sapiens 12-19 26552919-5 2015 Celastrol"s miR-223 induction might be due to NF-kappaB inhibition and transient mTOR activation: these two events occurred prior to miR-223 elevation in celastrol-treated cells. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 81-85 26552919-5 2015 Celastrol"s miR-223 induction might be due to NF-kappaB inhibition and transient mTOR activation: these two events occurred prior to miR-223 elevation in celastrol-treated cells. celastrol 0-9 microRNA 223 Homo sapiens 133-140 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 26-35 microRNA 223 Homo sapiens 50-57 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 26-35 microRNA 223 Homo sapiens 76-83 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 26-35 mechanistic target of rapamycin kinase Homo sapiens 146-150 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 110-119 microRNA 223 Homo sapiens 50-57 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 110-119 microRNA 223 Homo sapiens 76-83 26552919-6 2015 NF-kappaB inhibitor, like celastrol, could induce miR-223; the induction of miR-223 by NF-kappaB inhibitor or celastrol was reduced by the use of mTOR inhibitor. celastrol 110-119 mechanistic target of rapamycin kinase Homo sapiens 146-150 26552919-7 2015 Finally and interestingly, miR-223 also could affect NF-kappaB and mTOR and the effects were different between cells treated or not treated with celastrol, thus providing an explanation for differing effects of miR-223 alteration on cellular viability in the presence of celastrol or not. celastrol 145-154 microRNA 223 Homo sapiens 27-34 26552919-7 2015 Finally and interestingly, miR-223 also could affect NF-kappaB and mTOR and the effects were different between cells treated or not treated with celastrol, thus providing an explanation for differing effects of miR-223 alteration on cellular viability in the presence of celastrol or not. celastrol 145-154 mechanistic target of rapamycin kinase Homo sapiens 67-71 26552919-7 2015 Finally and interestingly, miR-223 also could affect NF-kappaB and mTOR and the effects were different between cells treated or not treated with celastrol, thus providing an explanation for differing effects of miR-223 alteration on cellular viability in the presence of celastrol or not. celastrol 145-154 microRNA 223 Homo sapiens 211-218 26552919-7 2015 Finally and interestingly, miR-223 also could affect NF-kappaB and mTOR and the effects were different between cells treated or not treated with celastrol, thus providing an explanation for differing effects of miR-223 alteration on cellular viability in the presence of celastrol or not. celastrol 271-280 microRNA 223 Homo sapiens 27-34 26552919-8 2015 CONCLUSIONS: For the first time, we disclose that celastrol could induce miR-223 in breast and prostate cancer cells, and that inhibiting miR-223 could further reduce the living cells in celastrol-treated cancer cell lines. celastrol 50-59 microRNA 223 Homo sapiens 73-80 26552919-8 2015 CONCLUSIONS: For the first time, we disclose that celastrol could induce miR-223 in breast and prostate cancer cells, and that inhibiting miR-223 could further reduce the living cells in celastrol-treated cancer cell lines. celastrol 187-196 microRNA 223 Homo sapiens 138-145 26344102-0 2015 Celastrol Protects against Obesity and Metabolic Dysfunction through Activation of a HSF1-PGC1alpha Transcriptional Axis. celastrol 0-9 heat shock factor 1 Mus musculus 85-89 26391399-7 2015 Additional Hsp90 inhibitors, including 17-(allylamino)-17-demethoxygeldanamycin, celastrol, and novobiocin also suppressed PMA-induced H1R gene up-regulation. celastrol 81-90 heat shock protein 90 alpha family class A member 1 Homo sapiens 11-16 26391399-7 2015 Additional Hsp90 inhibitors, including 17-(allylamino)-17-demethoxygeldanamycin, celastrol, and novobiocin also suppressed PMA-induced H1R gene up-regulation. celastrol 81-90 histamine receptor H1 Homo sapiens 135-138 26500453-0 2015 Celastrol induces cell cycle arrest by MicroRNA-21-mTOR-mediated inhibition p27 protein degradation in gastric cancer. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 51-55 26500453-0 2015 Celastrol induces cell cycle arrest by MicroRNA-21-mTOR-mediated inhibition p27 protein degradation in gastric cancer. celastrol 0-9 interferon alpha inducible protein 27 Homo sapiens 76-79 26500453-8 2015 RESULTS: Celastrol caused G2/M cell-cycle arrest that was accompanied by the down-regulation of miR-21 expression. celastrol 9-18 microRNA 21 Homo sapiens 96-102 26500453-9 2015 In particular, miR-21 overexpression reversed cell cycle arrest effects of celastrol. celastrol 75-84 microRNA 21 Homo sapiens 15-21 26500453-10 2015 Further study showed that celastrol increased levels of the p27 protein by inhibiting its degradation. celastrol 26-35 interferon alpha inducible protein 27 Homo sapiens 60-63 26500453-11 2015 miR-21 and mTOR signaling pathway was involved in the increase of p27 protein expression in BGC-823 and MGC-803 cells treated with celastrol. celastrol 131-140 microRNA 21 Homo sapiens 0-6 26500453-11 2015 miR-21 and mTOR signaling pathway was involved in the increase of p27 protein expression in BGC-823 and MGC-803 cells treated with celastrol. celastrol 131-140 mechanistic target of rapamycin kinase Homo sapiens 11-15 26500453-11 2015 miR-21 and mTOR signaling pathway was involved in the increase of p27 protein expression in BGC-823 and MGC-803 cells treated with celastrol. celastrol 131-140 interferon alpha inducible protein 27 Homo sapiens 66-69 26500453-12 2015 Significantly, miR-21 overexpression restored the decrease of mTOR activity in cells exposed celastrol. celastrol 93-102 microRNA 21 Homo sapiens 15-21 26500453-12 2015 Significantly, miR-21 overexpression restored the decrease of mTOR activity in cells exposed celastrol. celastrol 93-102 mechanistic target of rapamycin kinase Homo sapiens 62-66 26500453-13 2015 CONCLUSIONS: The effect of celastrol on cell cycle arrest of gastric cancer cells was due to an increase of p27 protein level via inhibiting miR-21-mTOR signaling pathway. celastrol 27-36 interferon alpha inducible protein 27 Homo sapiens 108-111 26500453-13 2015 CONCLUSIONS: The effect of celastrol on cell cycle arrest of gastric cancer cells was due to an increase of p27 protein level via inhibiting miR-21-mTOR signaling pathway. celastrol 27-36 microRNA 21 Homo sapiens 141-147 26500453-13 2015 CONCLUSIONS: The effect of celastrol on cell cycle arrest of gastric cancer cells was due to an increase of p27 protein level via inhibiting miR-21-mTOR signaling pathway. celastrol 27-36 mechanistic target of rapamycin kinase Homo sapiens 148-152 26447544-5 2015 Treatment with celastrol alone led to the decreased expressions of HSP90 client proteins including survivin, AKT, EGFR, which was enhanced by the addition of triptolide. celastrol 15-24 heat shock protein 90 alpha family class A member 1 Homo sapiens 67-72 26447544-5 2015 Treatment with celastrol alone led to the decreased expressions of HSP90 client proteins including survivin, AKT, EGFR, which was enhanced by the addition of triptolide. celastrol 15-24 AKT serine/threonine kinase 1 Homo sapiens 109-112 26447544-5 2015 Treatment with celastrol alone led to the decreased expressions of HSP90 client proteins including survivin, AKT, EGFR, which was enhanced by the addition of triptolide. celastrol 15-24 epidermal growth factor receptor Homo sapiens 114-118 26447544-6 2015 Additionally, the celastrol-induced expression of HSP70 and HSP27 was abrogated by triptolide. celastrol 18-27 heat shock protein family A (Hsp70) member 4 Homo sapiens 50-55 26447544-6 2015 Additionally, the celastrol-induced expression of HSP70 and HSP27 was abrogated by triptolide. celastrol 18-27 heat shock protein family B (small) member 1 Homo sapiens 60-65 26474287-0 2015 Direct inhibition of c-Myc-Max heterodimers by celastrol and celastrol-inspired triterpenoids. celastrol 47-56 MYC proto-oncogene, bHLH transcription factor Homo sapiens 21-26 26474287-0 2015 Direct inhibition of c-Myc-Max heterodimers by celastrol and celastrol-inspired triterpenoids. celastrol 61-70 MYC proto-oncogene, bHLH transcription factor Homo sapiens 21-26 26474287-3 2015 We report here that the naturally-occurring triterpenoid celastrol is an inhibitor of the c-Myc (Myc) oncoprotein, which is over-expressed in many human cancers. celastrol 57-66 MYC proto-oncogene, bHLH transcription factor Homo sapiens 90-95 26474287-3 2015 We report here that the naturally-occurring triterpenoid celastrol is an inhibitor of the c-Myc (Myc) oncoprotein, which is over-expressed in many human cancers. celastrol 57-66 MYC proto-oncogene, bHLH transcription factor Homo sapiens 92-95 26474287-11 2015 These studies indicate that certain pharmacologically undesirable properties of celastrol such as Michael adduct formation can be eliminated while increasing selectivity and potency toward Myc and N-Myc. celastrol 80-89 MYC proto-oncogene, bHLH transcription factor Homo sapiens 189-192 26474287-11 2015 These studies indicate that certain pharmacologically undesirable properties of celastrol such as Michael adduct formation can be eliminated while increasing selectivity and potency toward Myc and N-Myc. celastrol 80-89 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 197-202 26344102-0 2015 Celastrol Protects against Obesity and Metabolic Dysfunction through Activation of a HSF1-PGC1alpha Transcriptional Axis. celastrol 0-9 peroxisome proliferative activated receptor, gamma, coactivator 1 alpha Mus musculus 90-99 26344102-4 2015 Genetic modulation of HSF1 levels altered white fat remodeling and thermogenesis, and pharmacological activation of HSF1 via celastrol was associated with enhanced energy expenditure, increased mitochondrial function in fat and muscle and protection against obesity, insulin resistance, and hepatic steatosis during high-fat diet regimens. celastrol 125-134 heat shock factor 1 Mus musculus 116-120 26344102-5 2015 The beneficial metabolic changes elicited by celastrol were abrogated in HSF1 knockout mice. celastrol 45-54 heat shock factor 1 Mus musculus 73-77 26344102-6 2015 Overall, our findings identify the temperature sensor HSF1 as a regulator of energy metabolism and demonstrate that augmenting HSF1 via celastrol represents a possible therapeutic strategy to treat obesity and its myriad metabolic consequences. celastrol 136-145 heat shock factor 1 Mus musculus 127-131 26165547-6 2015 The effect of celastrol on the apoptotic rate of the cells was evaluated by flow cytometry using Annexin V-PE/7-AAD staining assay. celastrol 14-23 annexin A5 Homo sapiens 97-106 26227505-6 2015 Recently, several plant-derived small molecules have been discovered exhibiting inhibitory activity towards Hsp90, such as epigallocatechin gallate, gedunin, lentiginosine, celastrol, and deguelin. celastrol 173-182 heat shock protein 90 alpha family class A member 1 Homo sapiens 108-113 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 cytochrome c, somatic Homo sapiens 105-117 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 BCL2 apoptosis regulator Homo sapiens 147-152 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 caspase 3 Homo sapiens 218-234 26165547-10 2015 Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. celastrol 30-39 collagen type XI alpha 2 chain Homo sapiens 250-254 25891850-0 2015 Celastrol induces proteasomal degradation of FANCD2 to sensitize lung cancer cells to DNA crosslinking agents. celastrol 0-9 FA complementation group D2 Homo sapiens 45-51 26116162-0 2015 Celastrol blocks binding of lipopolysaccharides to a Toll-like receptor4/myeloid differentiation factor2 complex in a thiol-dependent manner. celastrol 0-9 toll-like receptor 4 Mus musculus 53-72 26116162-3 2015 AIM OF THE STUDY: We investigated whether celastrol suppressed binding of lipopolysaccharides (LPS) to myeloid differentiation factor 2 (MD2), thereby downregulating Toll-like receptor4 (TLR4) activation in mouse primary macrophages. celastrol 42-51 lymphocyte antigen 96 Mus musculus 103-135 26116162-3 2015 AIM OF THE STUDY: We investigated whether celastrol suppressed binding of lipopolysaccharides (LPS) to myeloid differentiation factor 2 (MD2), thereby downregulating Toll-like receptor4 (TLR4) activation in mouse primary macrophages. celastrol 42-51 lymphocyte antigen 96 Mus musculus 137-140 26116162-3 2015 AIM OF THE STUDY: We investigated whether celastrol suppressed binding of lipopolysaccharides (LPS) to myeloid differentiation factor 2 (MD2), thereby downregulating Toll-like receptor4 (TLR4) activation in mouse primary macrophages. celastrol 42-51 toll-like receptor 4 Mus musculus 166-185 26116162-3 2015 AIM OF THE STUDY: We investigated whether celastrol suppressed binding of lipopolysaccharides (LPS) to myeloid differentiation factor 2 (MD2), thereby downregulating Toll-like receptor4 (TLR4) activation in mouse primary macrophages. celastrol 42-51 toll-like receptor 4 Mus musculus 187-191 26116162-8 2015 Celastrol suppressed LPS binding to MD2, as shown by the in vitro binding assay, whereas it did not inhibit TBK1. celastrol 0-9 lymphocyte antigen 96 Mus musculus 36-39 26116162-9 2015 In addition, co-localization of LPS with MD2 in BMDMs was blocked by celastrol. celastrol 69-78 lymphocyte antigen 96 Mus musculus 41-44 26116162-10 2015 The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages. celastrol 26-35 lymphocyte antigen 96 Mus musculus 54-57 26116162-10 2015 The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages. celastrol 26-35 toll-like receptor 4 Mus musculus 221-225 26116162-10 2015 The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages. celastrol 170-179 lymphocyte antigen 96 Mus musculus 54-57 26116162-10 2015 The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages. celastrol 170-179 toll-like receptor 4 Mus musculus 221-225 26116162-11 2015 CONCLUSION: Our results demonstrate that celastrol suppresses TLR4 activation through the inhibition of LPS binding to the TLR4/MD2 complex. celastrol 41-50 toll-like receptor 4 Mus musculus 62-66 26116162-11 2015 CONCLUSION: Our results demonstrate that celastrol suppresses TLR4 activation through the inhibition of LPS binding to the TLR4/MD2 complex. celastrol 41-50 toll-like receptor 4 Mus musculus 123-127 26116162-11 2015 CONCLUSION: Our results demonstrate that celastrol suppresses TLR4 activation through the inhibition of LPS binding to the TLR4/MD2 complex. celastrol 41-50 lymphocyte antigen 96 Mus musculus 128-131 26126538-2 2015 The expression of HDAC3 was decreased in cancer cell lines resistant to anti-cancer drugs such as celastrol and taxol. celastrol 98-107 histone deacetylase 3 Homo sapiens 18-23 28717468-0 2015 Natural products triptolide, celastrol, and withaferin A inhibit the chaperone activity of peroxiredoxin I. celastrol 29-38 peroxiredoxin 1 Homo sapiens 91-106 28717468-6 2015 We have also identified celastrol and withaferin A as novel Prx I chaperone inhibitors that are even more potent than triptolide in the chaperone activity assay. celastrol 24-33 peroxiredoxin 1 Homo sapiens 60-65 25891850-3 2015 In the present study, we aimed to identify FANCD2-targeting agents, and found that the natural compound celastrol induced degradation of FANCD2 through the ubiquitin-proteasome pathway. celastrol 104-113 FA complementation group D2 Homo sapiens 43-49 25891850-3 2015 In the present study, we aimed to identify FANCD2-targeting agents, and found that the natural compound celastrol induced degradation of FANCD2 through the ubiquitin-proteasome pathway. celastrol 104-113 FA complementation group D2 Homo sapiens 137-143 25891850-4 2015 We demonstrated that celastrol downregulated the basal and DNA damaging agent-induced monoubiquitination of FANCD2, followed by proteolytic degradation of the substrate. celastrol 21-30 FA complementation group D2 Homo sapiens 108-114 25891850-5 2015 Furthermore, celastrol treatment abrogated the G2 checkpoint induced by IR, and enhanced the ICL agent-induced DNA damage and inhibitory effects on lung cancer cells through depletion of FANCD2. celastrol 13-22 FA complementation group D2 Homo sapiens 187-193 25891850-6 2015 These results indicate that celastrol is a FANCD2 inhibitor that could interfere with the monoubiquitination and protein stability of FANCD2, providing a novel opportunity to develop FA pathway inhibitor and combinational therapy for malignant neoplasms. celastrol 28-37 FA complementation group D2 Homo sapiens 43-49 25891850-6 2015 These results indicate that celastrol is a FANCD2 inhibitor that could interfere with the monoubiquitination and protein stability of FANCD2, providing a novel opportunity to develop FA pathway inhibitor and combinational therapy for malignant neoplasms. celastrol 28-37 FA complementation group D2 Homo sapiens 134-140 25818165-0 2015 Anticancer effect of celastrol on human triple negative breast cancer: possible involvement of oxidative stress, mitochondrial dysfunction, apoptosis and PI3K/Akt pathways. celastrol 21-30 AKT serine/threonine kinase 1 Homo sapiens 159-162 26109308-8 2015 The results showed that celastrol inhibited adhesion, migration and invasion of ECA-109 cells and expressions of integrins beta1, beta4, alphav and beta-Catenin, LRP6 in Wnt signal pathway in a dose-dependent manner. celastrol 24-33 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 123-135 26109308-8 2015 The results showed that celastrol inhibited adhesion, migration and invasion of ECA-109 cells and expressions of integrins beta1, beta4, alphav and beta-Catenin, LRP6 in Wnt signal pathway in a dose-dependent manner. celastrol 24-33 catenin beta 1 Homo sapiens 148-160 26109308-8 2015 The results showed that celastrol inhibited adhesion, migration and invasion of ECA-109 cells and expressions of integrins beta1, beta4, alphav and beta-Catenin, LRP6 in Wnt signal pathway in a dose-dependent manner. celastrol 24-33 LDL receptor related protein 6 Homo sapiens 162-166 25818165-11 2015 PI3K/Akt/mTOR inhibitor, PF-04691502 and mTOR inhibitor rapamycin enhanced the apoptosis-inducing effect of celastrol. celastrol 108-117 AKT serine/threonine kinase 1 Homo sapiens 5-8 25818165-5 2015 Celastrol induced apoptosis in TNBC cells, were supported by DNA fragmentation, caspase-3 activation and PARP cleavage. celastrol 0-9 caspase 3 Homo sapiens 80-89 25818165-11 2015 PI3K/Akt/mTOR inhibitor, PF-04691502 and mTOR inhibitor rapamycin enhanced the apoptosis-inducing effect of celastrol. celastrol 108-117 mechanistic target of rapamycin kinase Homo sapiens 9-13 25818165-5 2015 Celastrol induced apoptosis in TNBC cells, were supported by DNA fragmentation, caspase-3 activation and PARP cleavage. celastrol 0-9 collagen type XI alpha 2 chain Homo sapiens 105-109 25818165-11 2015 PI3K/Akt/mTOR inhibitor, PF-04691502 and mTOR inhibitor rapamycin enhanced the apoptosis-inducing effect of celastrol. celastrol 108-117 mechanistic target of rapamycin kinase Homo sapiens 41-45 25818165-12 2015 These data demonstrated that celastrol induces apoptosis in TNBC cells and indicated that apoptosis might be mediated through mitochondrial dysfunction and PI3K/Akt signaling pathway. celastrol 29-38 AKT serine/threonine kinase 1 Homo sapiens 161-164 25818165-6 2015 Meanwhile, celastrol triggered reactive oxygen species production with collapse of mitochondrial membrane potential, down-regulation of Bcl-2 and up-regulation of Bax expression. celastrol 11-20 BCL2 apoptosis regulator Homo sapiens 136-141 25818165-6 2015 Meanwhile, celastrol triggered reactive oxygen species production with collapse of mitochondrial membrane potential, down-regulation of Bcl-2 and up-regulation of Bax expression. celastrol 11-20 BCL2 associated X, apoptosis regulator Homo sapiens 163-166 25818165-7 2015 Celastrol effectively decreased PI3K 110alpha/85alpha enzyme activity, phosphorylation of Akt(ser473) and p70S6K1 and 4E-BP1. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 90-93 25818165-7 2015 Celastrol effectively decreased PI3K 110alpha/85alpha enzyme activity, phosphorylation of Akt(ser473) and p70S6K1 and 4E-BP1. celastrol 0-9 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 106-124 25818165-9 2015 It clearly indicates that celastrol acts through PI3k/Akt/mTOR axis. celastrol 26-35 AKT serine/threonine kinase 1 Homo sapiens 54-57 25818165-9 2015 It clearly indicates that celastrol acts through PI3k/Akt/mTOR axis. celastrol 26-35 mechanistic target of rapamycin kinase Homo sapiens 58-62 25818165-10 2015 We also found that celastrol inhibited the Akt/GSK3beta and Akt/NFkB survival pathway. celastrol 19-28 AKT serine/threonine kinase 1 Homo sapiens 43-46 25818165-10 2015 We also found that celastrol inhibited the Akt/GSK3beta and Akt/NFkB survival pathway. celastrol 19-28 glycogen synthase kinase 3 beta Homo sapiens 47-55 25818165-10 2015 We also found that celastrol inhibited the Akt/GSK3beta and Akt/NFkB survival pathway. celastrol 19-28 AKT serine/threonine kinase 1 Homo sapiens 60-63 25359574-0 2015 ATF2 contributes to cisplatin resistance in non-small cell lung cancer and celastrol induces cisplatin resensitization through inhibition of JNK/ATF2 pathway. celastrol 75-84 mitogen-activated protein kinase 8 Homo sapiens 141-144 25359574-0 2015 ATF2 contributes to cisplatin resistance in non-small cell lung cancer and celastrol induces cisplatin resensitization through inhibition of JNK/ATF2 pathway. celastrol 75-84 activating transcription factor 2 Homo sapiens 145-149 25359574-6 2015 Celastrol-mediated ATF2/cJUN activity was measured. celastrol 0-9 activating transcription factor 2 Homo sapiens 19-23 25359574-6 2015 Celastrol-mediated ATF2/cJUN activity was measured. celastrol 0-9 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-28 25359574-9 2015 By contrast, Celastrol-mediated ATF2/cJUN functional inhibition restored the response to CDDP. celastrol 13-22 activating transcription factor 2 Homo sapiens 32-36 25359574-9 2015 By contrast, Celastrol-mediated ATF2/cJUN functional inhibition restored the response to CDDP. celastrol 13-22 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-41 25359574-13 2015 Altogether, our results indicate a potential increase in CDDP sensitivity, on Celastrol-mediated ATF2/cJUN inhibition. celastrol 78-87 activating transcription factor 2 Homo sapiens 97-101 25359574-13 2015 Altogether, our results indicate a potential increase in CDDP sensitivity, on Celastrol-mediated ATF2/cJUN inhibition. celastrol 78-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-106 25858875-0 2015 Celastrol ameliorates experimental colitis in IL-10 deficient mice via the up-regulation of autophagy. celastrol 0-9 interleukin 10 Mus musculus 46-51 25961164-0 2015 Celastrol Protects against Antimycin A-Induced Insulin Resistance in Human Skeletal Muscle Cells. celastrol 0-9 insulin Homo sapiens 47-54 25961164-2 2015 The aim of the present study was to evaluate the functional roles of an anti-inflammatory compound, celastrol, in mitochondrial dysfunction and insulin resistance induced by antimycin A (AMA) in human skeletal muscle cells. celastrol 100-109 insulin Homo sapiens 144-151 25961164-3 2015 We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. celastrol 14-23 insulin Homo sapiens 43-50 25961164-3 2015 We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. celastrol 14-23 AKT serine/threonine kinase 1 Homo sapiens 128-131 25961164-5 2015 Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-kappaB and PKC theta activation in human skeletal muscle treated with AMA. celastrol 0-9 insulin Homo sapiens 61-68 25961164-5 2015 Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-kappaB and PKC theta activation in human skeletal muscle treated with AMA. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 117-121 25961164-6 2015 The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. celastrol 49-58 insulin Homo sapiens 19-26 25961164-6 2015 The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. celastrol 49-58 solute carrier family 2 member 4 Homo sapiens 93-98 25961164-7 2015 Taken together, these results suggest that celastrol may be advocated for use as a potential therapeutic molecule to protect against mitochondrial dysfunction-induced insulin resistance in human skeletal muscle cells. celastrol 43-52 insulin Homo sapiens 167-174 25858875-8 2015 RESULTS: The one-week administration of celastrol ameliorated established colitis in IL-10 deficient mice, associated with a reduction of marked histological inflammation, a decreased colon MPO concentration and suppression of colonic proinflammatory cytokine. celastrol 40-49 interleukin 10 Mus musculus 85-90 25858875-8 2015 RESULTS: The one-week administration of celastrol ameliorated established colitis in IL-10 deficient mice, associated with a reduction of marked histological inflammation, a decreased colon MPO concentration and suppression of colonic proinflammatory cytokine. celastrol 40-49 myeloperoxidase Mus musculus 190-193 26000480-5 2015 Celastrol suppresses food intake, blocks reduction of energy expenditure, and leads to up to 45% weight loss in hyperleptinemic diet-induced obese (DIO) mice by increasing leptin sensitivity, but it is ineffective in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mouse models. celastrol 0-9 leptin receptor Mus musculus 235-261 25858875-10 2015 The Western blotting analysis of the PI3K/Akt/mTOR pathway and autophagy showed that celastrol treatment up-regulated the autophagy of colon tissue by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 85-94 thymoma viral proto-oncogene 1 Mus musculus 42-45 25858875-2 2015 This study was aimed to investigate whether celastrol could ameliorate the inflammation of IL-10 deficient mice, a murine model of Crohn"s disease (CD) with the induction of autophagy. celastrol 44-53 interleukin 10 Mus musculus 91-96 25858875-10 2015 The Western blotting analysis of the PI3K/Akt/mTOR pathway and autophagy showed that celastrol treatment up-regulated the autophagy of colon tissue by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 85-94 mechanistic target of rapamycin kinase Mus musculus 46-50 25611379-0 2015 Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells: an in vitro and in vivo study. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 54-57 25858875-10 2015 The Western blotting analysis of the PI3K/Akt/mTOR pathway and autophagy showed that celastrol treatment up-regulated the autophagy of colon tissue by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 85-94 thymoma viral proto-oncogene 1 Mus musculus 172-175 25858875-10 2015 The Western blotting analysis of the PI3K/Akt/mTOR pathway and autophagy showed that celastrol treatment up-regulated the autophagy of colon tissue by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 85-94 mechanistic target of rapamycin kinase Mus musculus 176-180 25858875-11 2015 CONCLUSIONS: Celastrol ameliorates experimental colitis in IL-10 deficient mice via the up-regulation of autophagy by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 13-22 interleukin 10 Mus musculus 59-64 25858875-11 2015 CONCLUSIONS: Celastrol ameliorates experimental colitis in IL-10 deficient mice via the up-regulation of autophagy by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 13-22 thymoma viral proto-oncogene 1 Mus musculus 139-142 25858875-11 2015 CONCLUSIONS: Celastrol ameliorates experimental colitis in IL-10 deficient mice via the up-regulation of autophagy by suppressing the PI3K/Akt/mTOR signaling pathway. celastrol 13-22 mechanistic target of rapamycin kinase Mus musculus 143-147 25903958-0 2015 Celastrol overcomes HSP72 gene silencing-mediated muscle atrophy and induces myofiber preservation. celastrol 0-9 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 20-25 25903958-5 2015 CEL treatment, however, markedly increased the HSP72 expression and rendered the myotube size recovered to the NC level even in the siRNA-treated cells. celastrol 0-3 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 47-52 25903958-6 2015 Moreover, the HSP72 siRNA upregulated forkhead box O3 (FoxO3) expression in the nucleus while CEL increased p-FoxO3 exclusively in the cytoplasm, thus leaving the p-FoxO3/FoxO3 balanced to the NC level by siRNA + CEL treatment. celastrol 94-97 forkhead box O3 Rattus norvegicus 110-115 25903958-6 2015 Moreover, the HSP72 siRNA upregulated forkhead box O3 (FoxO3) expression in the nucleus while CEL increased p-FoxO3 exclusively in the cytoplasm, thus leaving the p-FoxO3/FoxO3 balanced to the NC level by siRNA + CEL treatment. celastrol 94-97 forkhead box O3 Rattus norvegicus 110-115 25903958-6 2015 Moreover, the HSP72 siRNA upregulated forkhead box O3 (FoxO3) expression in the nucleus while CEL increased p-FoxO3 exclusively in the cytoplasm, thus leaving the p-FoxO3/FoxO3 balanced to the NC level by siRNA + CEL treatment. celastrol 94-97 forkhead box O3 Rattus norvegicus 110-115 25571843-0 2015 Celastrol prevents circulatory failure via induction of heme oxygenase-1 and heat shock protein 70 in endotoxemic rats. celastrol 0-9 heme oxygenase 1 Rattus norvegicus 56-72 25571843-0 2015 Celastrol prevents circulatory failure via induction of heme oxygenase-1 and heat shock protein 70 in endotoxemic rats. celastrol 0-9 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 77-98 25571843-10 2015 The plasma levels of ALT, LDH, TNF-alpha, and nitric oxide metabolites increased markedly during sepsis, which significantly reduced after celastrol treatments. celastrol 139-148 tumor necrosis factor Rattus norvegicus 31-40 25571843-11 2015 Celastrol attenuated iNOS, TNF-alpha, NF-kappaB phospho-p65 expression, superoxide anion production, and caspase 3 activity in the cardiovascular system, all of which were markedly elevated after LPS challenge. celastrol 0-9 nitric oxide synthase 2 Rattus norvegicus 21-25 25571843-11 2015 Celastrol attenuated iNOS, TNF-alpha, NF-kappaB phospho-p65 expression, superoxide anion production, and caspase 3 activity in the cardiovascular system, all of which were markedly elevated after LPS challenge. celastrol 0-9 tumor necrosis factor Rattus norvegicus 27-36 25571843-11 2015 Celastrol attenuated iNOS, TNF-alpha, NF-kappaB phospho-p65 expression, superoxide anion production, and caspase 3 activity in the cardiovascular system, all of which were markedly elevated after LPS challenge. celastrol 0-9 caspase 3 Rattus norvegicus 105-114 25571843-12 2015 Furthermore, celastrol induced HO-1 and HSP70 expressions increase in nuclear levels of Nrf2 and HSF-1, respectively, and increase cardiac GSH level 8h after LPS challenge. celastrol 13-22 heme oxygenase 1 Rattus norvegicus 31-35 25571843-12 2015 Furthermore, celastrol induced HO-1 and HSP70 expressions increase in nuclear levels of Nrf2 and HSF-1, respectively, and increase cardiac GSH level 8h after LPS challenge. celastrol 13-22 NFE2 like bZIP transcription factor 2 Rattus norvegicus 88-92 25571843-12 2015 Furthermore, celastrol induced HO-1 and HSP70 expressions increase in nuclear levels of Nrf2 and HSF-1, respectively, and increase cardiac GSH level 8h after LPS challenge. celastrol 13-22 heat shock transcription factor 1 Rattus norvegicus 97-102 25571843-14 2015 Induction of HO-1 and HSP70 by celastrol participates in these beneficial effects. celastrol 31-40 heme oxygenase 1 Rattus norvegicus 13-17 25776492-4 2015 The accumulation of daunorubicin or rhodamine 123, fluorescent substrates of P-glycoprotein, in KB/MDR1 cells increased in the presence of caffeic acid phenetyl ester (CAPE), licochalcone A, anacardic acid, celastrol, xanthohumol, magnolol, and honokiol in a concentration-dependent manner. celastrol 207-216 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 25776492-6 2015 The ATPase activities of P-glycoprotein were stimulated by CAPE, licochalcone A, anacardic acid, celastrol, xanthohumol, magnolol, and honokiol. celastrol 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 25336054-6 2015 Examination of the underlying mechanisms indicated that the effect of tripterine is mediated by the induction of heat shock protein 32 expression and the inhibition of JNK activation. celastrol 70-80 mitogen-activated protein kinase 8 Mus musculus 168-171 25059279-4 2015 In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. celastrol 38-47 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 152-168 25059279-5 2015 Furthermore, celastrol significantly suppressed cytokine- induced signaling cascades leading to nuclear factor kappa B (NF-kappaB) activation, including IkappaB-kinase (IKK) activation, IkappaB degradation, p65 phosphorylation, and p65 DNA binding activity. celastrol 13-22 synaptotagmin 1 Rattus norvegicus 207-210 25059279-5 2015 Furthermore, celastrol significantly suppressed cytokine- induced signaling cascades leading to nuclear factor kappa B (NF-kappaB) activation, including IkappaB-kinase (IKK) activation, IkappaB degradation, p65 phosphorylation, and p65 DNA binding activity. celastrol 13-22 synaptotagmin 1 Rattus norvegicus 232-235 25529994-0 2015 Celastrol attenuates bone erosion in collagen-Induced arthritis mice and inhibits osteoclast differentiation and function in RANKL-induced RAW264.7. celastrol 0-9 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 125-130 25529994-6 2015 When RAW264.7 cells were treated with RANKL, celastrol inhibited the formation of TRAP+ multinucleated cells and the bone-resorbing activity in dose-dependent manners. celastrol 45-54 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 38-43 25529994-6 2015 When RAW264.7 cells were treated with RANKL, celastrol inhibited the formation of TRAP+ multinucleated cells and the bone-resorbing activity in dose-dependent manners. celastrol 45-54 acid phosphatase 5, tartrate resistant Mus musculus 82-86 25529994-7 2015 Furthermore, celastrol reduced the RANKL-induced expression of osteoclastic genes and transcriptional factors, as well as phosphorylation of NF-kB and mitogen-activated protein kinases (MAPK). celastrol 13-22 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 35-40 25611379-5 2015 Exposure to celastrol resulted in the activation of caspase-3, -8, and -9, indicating that celastrol induced apoptosis through both extrinsic and intrinsic pathways. celastrol 12-21 caspase 3 Homo sapiens 52-73 25611379-5 2015 Exposure to celastrol resulted in the activation of caspase-3, -8, and -9, indicating that celastrol induced apoptosis through both extrinsic and intrinsic pathways. celastrol 91-100 caspase 3 Homo sapiens 52-73 25611379-9 2015 Celastrol also induced JNK activation and ROS generation. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 23-26 25611379-10 2015 The JNK inhibitor significantly attenuated celastrol-triggered apoptosis and autophagy while ROS scavenger could completely reverse them. celastrol 43-52 mitogen-activated protein kinase 8 Homo sapiens 4-7 25611379-14 2015 Taken together, our results revealed that celastrol caused G2/M phase arrest, induced apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells. celastrol 42-51 mitogen-activated protein kinase 8 Homo sapiens 122-125 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 10-19 cytochrome c, somatic Homo sapiens 43-55 25139619-7 2015 Biochemical and genetic assays using OSCC cells and modified murine embryonic fibroblasts demonstrated that intact PERK-eIF2-ATF4-CHOP signaling is required for pro-apoptotic UPR and OSCC death following celastrol treatment. celastrol 204-213 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 115-119 25139619-7 2015 Biochemical and genetic assays using OSCC cells and modified murine embryonic fibroblasts demonstrated that intact PERK-eIF2-ATF4-CHOP signaling is required for pro-apoptotic UPR and OSCC death following celastrol treatment. celastrol 204-213 eukaryotic translation initiation factor 2, subunit 2 (beta) Mus musculus 120-124 25139619-7 2015 Biochemical and genetic assays using OSCC cells and modified murine embryonic fibroblasts demonstrated that intact PERK-eIF2-ATF4-CHOP signaling is required for pro-apoptotic UPR and OSCC death following celastrol treatment. celastrol 204-213 activating transcription factor 4 Mus musculus 125-129 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 10-19 caspase 3 Homo sapiens 88-97 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 10-19 caspase 9 Homo sapiens 102-111 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 129-138 cytochrome c, somatic Homo sapiens 43-55 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 129-138 caspase 3 Homo sapiens 88-97 25657108-5 2015 Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. celastrol 129-138 caspase 9 Homo sapiens 102-111 26402060-0 2015 Tripterine treatment improves endothelial progenitor cell function via integrin-linked kinase. celastrol 0-10 integrin linked kinase Mus musculus 71-93 25866772-0 2015 Effect of celastrol on growth inhibition of prostate cancer cells through the regulation of hERG channel in vitro. celastrol 10-19 ETS transcription factor ERG Homo sapiens 92-96 25866772-11 2015 Overexpression of hERG channel was found in DU145 cells, while Celastrol could downregulate it at both protein and mRNA level in a dose-dependent manner (P < 0.01). celastrol 63-72 ETS transcription factor ERG Homo sapiens 18-22 26402060-5 2015 Tripterine restored integrin-linked kinase (ILK) levels downregulated by ox-LDL in EPCs, suggesting the involvement of the ILK/Akt pathway. celastrol 0-10 integrin linked kinase Mus musculus 20-42 25866772-12 2015 CONCLUSIONS: Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel. celastrol 13-22 ETS transcription factor ERG Homo sapiens 128-132 25866772-12 2015 CONCLUSIONS: Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel. celastrol 13-22 ETS transcription factor ERG Homo sapiens 265-269 25866772-12 2015 CONCLUSIONS: Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel. celastrol 173-182 ETS transcription factor ERG Homo sapiens 128-132 26402060-5 2015 Tripterine restored integrin-linked kinase (ILK) levels downregulated by ox-LDL in EPCs, suggesting the involvement of the ILK/Akt pathway. celastrol 0-10 integrin linked kinase Mus musculus 44-47 25866772-12 2015 CONCLUSIONS: Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel. celastrol 173-182 ETS transcription factor ERG Homo sapiens 265-269 26402060-5 2015 Tripterine restored integrin-linked kinase (ILK) levels downregulated by ox-LDL in EPCs, suggesting the involvement of the ILK/Akt pathway. celastrol 0-10 integrin linked kinase Mus musculus 123-126 26402060-5 2015 Tripterine restored integrin-linked kinase (ILK) levels downregulated by ox-LDL in EPCs, suggesting the involvement of the ILK/Akt pathway. celastrol 0-10 thymoma viral proto-oncogene 1 Mus musculus 127-130 26402060-7 2015 In atherosclerotic mice injected with green fluorescent protein-labeled EPCs to evaluate EPC function, tripterine decreased aortic lesions and plaque deposition, and injection of tripterine-treated EPCs restored ILK levels. celastrol 179-189 integrin linked kinase Mus musculus 212-215 26402060-8 2015 CONCLUSION: The present results suggest that tripterine improves vascular function in atherosclerosis by enhancing EPC function through a mechanism involving the ILK signaling pathway. celastrol 45-55 integrin linked kinase Mus musculus 162-165 25355627-6 2015 Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression. celastrol 31-40 heat shock transcription factor 1 Homo sapiens 74-78 25941817-4 2015 We found that celastrol can completely inhibit neutrophil oxidative burst and NET formation induced by tumor necrosis factor alpha (TNFalpha) with an IC50 of 0.34 microM and by ovalbumin:anti-ovalbumin immune complexes (Ova IC) with an IC50 of 1.53 microM. celastrol 14-23 tumor necrosis factor Homo sapiens 103-130 25941817-4 2015 We found that celastrol can completely inhibit neutrophil oxidative burst and NET formation induced by tumor necrosis factor alpha (TNFalpha) with an IC50 of 0.34 microM and by ovalbumin:anti-ovalbumin immune complexes (Ova IC) with an IC50 of 1.53 microM. celastrol 14-23 tumor necrosis factor Homo sapiens 132-140 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 spleen associated tyrosine kinase Homo sapiens 133-136 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 mitogen-activated protein kinase kinase 7 Homo sapiens 224-227 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 mitogen-activated protein kinase 1 Homo sapiens 230-267 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 mitogen-activated protein kinase 1 Homo sapiens 269-272 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 NFKB inhibitor alpha Homo sapiens 279-303 25941817-6 2015 Further investigating into the mechanisms, we found that celastrol treatment downregulated the activation of spleen tyrosine kinase (SYK) and the concomitant phosphorylation of mitogen-activated protein kinase kinase (MAPKK/MEK), extracellular-signal-regulated kinase (ERK), and NFkappaB inhibitor alpha (IkappaBalpha), as well as citrullination of histones. celastrol 57-66 NFKB inhibitor alpha Homo sapiens 305-317 25941817-7 2015 Our data reveals that celastrol potently inhibits neutrophil oxidative burst and NET formation induced by different inflammatory stimuli, possibly through downregulating the SYK-MEK-ERK-NFkappaB signaling cascade. celastrol 22-31 spleen associated tyrosine kinase Homo sapiens 174-177 25941817-7 2015 Our data reveals that celastrol potently inhibits neutrophil oxidative burst and NET formation induced by different inflammatory stimuli, possibly through downregulating the SYK-MEK-ERK-NFkappaB signaling cascade. celastrol 22-31 mitogen-activated protein kinase kinase 7 Homo sapiens 178-181 25941817-7 2015 Our data reveals that celastrol potently inhibits neutrophil oxidative burst and NET formation induced by different inflammatory stimuli, possibly through downregulating the SYK-MEK-ERK-NFkappaB signaling cascade. celastrol 22-31 mitogen-activated protein kinase 1 Homo sapiens 182-185 25941817-7 2015 Our data reveals that celastrol potently inhibits neutrophil oxidative burst and NET formation induced by different inflammatory stimuli, possibly through downregulating the SYK-MEK-ERK-NFkappaB signaling cascade. celastrol 22-31 nuclear factor kappa B subunit 1 Homo sapiens 186-194 25989799-8 2015 Additionally, treatment with celastrol, which is also an inhibitor of the Hsp90-Cdc37 complex, decreased LRRK2 levels. celastrol 29-38 heat shock protein 90 alpha family class A member 1 Homo sapiens 74-79 25989799-8 2015 Additionally, treatment with celastrol, which is also an inhibitor of the Hsp90-Cdc37 complex, decreased LRRK2 levels. celastrol 29-38 cell division cycle 37, HSP90 cochaperone Homo sapiens 80-85 25989799-8 2015 Additionally, treatment with celastrol, which is also an inhibitor of the Hsp90-Cdc37 complex, decreased LRRK2 levels. celastrol 29-38 leucine rich repeat kinase 2 Homo sapiens 105-110 25989799-9 2015 Interestingly, treatment with WA in the presence of celastrol enhanced the clearance of LRRK2. celastrol 52-61 leucine rich repeat kinase 2 Homo sapiens 88-93 25355627-6 2015 Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression. celastrol 31-40 heat shock transcription factor 1 Homo sapiens 107-111 25355627-6 2015 Proteotoxic stressors, such as celastrol and MG132, are known to activate HSF1, and are potent inducers of HSF1 binding and IER5 expression. celastrol 31-40 immediate early response 5 Homo sapiens 124-128 25811791-0 2015 Inhibitory mechanisms of celastrol on human liver cytochrome P450 1A2, 2C19, 2D6, 2E1 and 3A4. celastrol 25-34 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 50-69 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 latexin Homo sapiens 123-126 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 128-134 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 latexin Homo sapiens 142-145 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 147-154 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 latexin Homo sapiens 142-145 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 167-173 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 latexin Homo sapiens 142-145 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 186-192 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 latexin Homo sapiens 142-145 25811791-5 2015 The results showed that celastrol inhibited the five types of human cytochrome P450 isoforms, with the IC50 values of 2.65 muM (CYP3A4), 5.99 muM (CYP2C19), 6.27 muM (CYP2D6), 7.66 muM (CYP1A2) and 9.38 muM (CYP2E1), respectively. celastrol 24-33 cytochrome P450 family 2 subfamily E member 1 Homo sapiens 208-214 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 24-33 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 180-186 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 24-33 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 244-251 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 24-33 latexin Homo sapiens 315-318 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 130-139 cytochrome P450 family 1 subfamily A member 2 Homo sapiens 180-186 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 130-139 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 244-251 25811791-6 2015 The data indicated that celastrol acted in different manners as an inhibitor of human cytochrome P450 isoforms, which showed that celastrol not only un-competitively inhibited the CYP1A2 and 2E1 activities, but also competitively inhibited the CYP2C19 and 2D6 activities with Ki values of 1.41, 2.29, 5.27 and 4.21 muM, respectively. celastrol 130-139 latexin Homo sapiens 315-318 25811791-7 2015 Celastrol was also a mixed-type inhibitor of CYP3A4, with Ki and Kis values of 2.02 and 5.49 muM, respectively. celastrol 0-9 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 45-51 25811791-7 2015 Celastrol was also a mixed-type inhibitor of CYP3A4, with Ki and Kis values of 2.02 and 5.49 muM, respectively. celastrol 0-9 latexin Homo sapiens 93-96 25310109-0 2014 Celastrol induces the apoptosis of breast cancer cells and inhibits their invasion via downregulation of MMP-9. celastrol 0-9 matrix metallopeptidase 9 Homo sapiens 105-110 25300680-7 2014 Comparing with model group, celastrol was able to effectively suppress weight and attenuate high fat mediated oxidative injury by improving ABCA1 expression, reducing the levels of TC, TG, LDL-c and Apo B in plasma, and increasing antioxidant enzymes activities and inhibiting NADPH oxidase activity, and decreasing the serum levels of Malondialdehyde (MDA) and reactive oxygen species in dose-dependent way. celastrol 28-37 ATP binding cassette subfamily A member 1 Rattus norvegicus 140-145 25300680-7 2014 Comparing with model group, celastrol was able to effectively suppress weight and attenuate high fat mediated oxidative injury by improving ABCA1 expression, reducing the levels of TC, TG, LDL-c and Apo B in plasma, and increasing antioxidant enzymes activities and inhibiting NADPH oxidase activity, and decreasing the serum levels of Malondialdehyde (MDA) and reactive oxygen species in dose-dependent way. celastrol 28-37 apolipoprotein B Rattus norvegicus 199-204 25474091-3 2014 In the present study, we sought to investigate the direct effects of celastrol (potent NF-kappaB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. celastrol 69-78 nuclear factor kappa B subunit 1 Homo sapiens 87-96 25474091-3 2014 In the present study, we sought to investigate the direct effects of celastrol (potent NF-kappaB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. celastrol 69-78 insulin Homo sapiens 147-154 24667175-6 2014 We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. celastrol 144-153 AKT serine/threonine kinase 1 Homo sapiens 101-104 24667175-6 2014 We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. celastrol 144-153 mechanistic target of rapamycin kinase Homo sapiens 106-110 24667175-6 2014 We also found an increase in phosphorylated AMPK following a decrease in all phosphorylated forms of AKT, mTOR and S6K after the treatment with celastrol. celastrol 144-153 ribosomal protein S6 kinase B1 Homo sapiens 115-118 25041185-4 2014 KEY RESULTS: In H9c2 cells, celastrol triggered reactive oxygen species (ROS) formation within minutes, induced nuclear translocation of the transcription factor heat shock factor 1 (HSF1) resulting in a heat shock response (HSR) leading to increased expression of heat shock proteins (HSPs). celastrol 28-37 heat shock transcription factor 1 Rattus norvegicus 162-181 25041185-4 2014 KEY RESULTS: In H9c2 cells, celastrol triggered reactive oxygen species (ROS) formation within minutes, induced nuclear translocation of the transcription factor heat shock factor 1 (HSF1) resulting in a heat shock response (HSR) leading to increased expression of heat shock proteins (HSPs). celastrol 28-37 heat shock transcription factor 1 Rattus norvegicus 183-187 25041185-6 2014 Celastrol improved H9c2 survival under hypoxic stress, and functional analysis revealed HSF1 and HO-1 as key effectors of the HSR, induced by celastrol, in promoting cytoprotection. celastrol 142-151 heat shock transcription factor 1 Rattus norvegicus 88-92 25041185-6 2014 Celastrol improved H9c2 survival under hypoxic stress, and functional analysis revealed HSF1 and HO-1 as key effectors of the HSR, induced by celastrol, in promoting cytoprotection. celastrol 142-151 heme oxygenase 1 Rattus norvegicus 97-101 25041185-8 2014 Celastrol triggered expression of cardioprotective HO-1 and inhibited fibrosis and infarct size. celastrol 0-9 heme oxygenase 1 Rattus norvegicus 51-55 25041185-10 2014 CONCLUSIONS AND IMPLICATIONS: Celastrol treatment induced an HSR through activation of HSF1 with up-regulation of HO-1 as the key effector, promoting cardiomyocyte survival, reduction of injury and adverse remodelling with preservation of cardiac function. celastrol 30-39 heat shock transcription factor 1 Rattus norvegicus 87-91 25041185-10 2014 CONCLUSIONS AND IMPLICATIONS: Celastrol treatment induced an HSR through activation of HSF1 with up-regulation of HO-1 as the key effector, promoting cardiomyocyte survival, reduction of injury and adverse remodelling with preservation of cardiac function. celastrol 30-39 heme oxygenase 1 Rattus norvegicus 114-118 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 tumor necrosis factor Homo sapiens 61-88 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 tumor necrosis factor Homo sapiens 90-99 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 caspase 8 Homo sapiens 143-152 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 caspase 3 Homo sapiens 154-163 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 collagen type XI alpha 2 chain Homo sapiens 168-172 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 baculoviral IAP repeat containing 2 Homo sapiens 296-301 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 baculoviral IAP repeat containing 3 Homo sapiens 306-311 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 CASP8 and FADD like apoptosis regulator Homo sapiens 323-347 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 BCL2 apoptosis regulator Homo sapiens 360-377 25310109-2 2014 In the present study, we reported that celastrol potentiated tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage, and inhibited the expression of anti-apoptotic proteins such as cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), cellular FLICE-inhibitory protein (FLIP), and B-cell lymphoma 2 (Bcl-2). celastrol 39-48 BCL2 apoptosis regulator Homo sapiens 379-384 25310109-3 2014 In addition, celastrol significantly reduced the invasion of MDA-MB-231 human breast cancer cells after TNF-alpha stimulation. celastrol 13-22 tumor necrosis factor Homo sapiens 104-113 25310109-4 2014 As matrix metalloproteinase-9 (MMP-9) plays a critical role in tumor metastasis, we analyzed its expression with celastrol treatment. celastrol 113-122 matrix metallopeptidase 9 Homo sapiens 3-29 25310109-4 2014 As matrix metalloproteinase-9 (MMP-9) plays a critical role in tumor metastasis, we analyzed its expression with celastrol treatment. celastrol 113-122 matrix metallopeptidase 9 Homo sapiens 31-36 25310109-5 2014 Western blot analysis and real-time PCR showed that celastrol dose-dependently suppressed TNF-alpha-induced MMP-9 gene expression at both the mRNA and protein levels in MDA-MB-231 cells. celastrol 52-61 tumor necrosis factor Homo sapiens 90-99 25310109-5 2014 Western blot analysis and real-time PCR showed that celastrol dose-dependently suppressed TNF-alpha-induced MMP-9 gene expression at both the mRNA and protein levels in MDA-MB-231 cells. celastrol 52-61 matrix metallopeptidase 9 Homo sapiens 108-113 25149175-5 2014 Inhibition of the IP3 receptor (IP3R) with 2-aminoethoxydiphenyl borate (2-APB) also effectively blocked celastrol-induced mitochondrial Ca2+ accumulation and subsequent paraptotic events. celastrol 105-114 inositol 1,4,5-trisphosphate receptor type 3 Homo sapiens 18-30 25383959-0 2014 Celastrol stimulates hypoxia-inducible factor-1 activity in tumor cells by initiating the ROS/Akt/p70S6K signaling pathway and enhancing hypoxia-inducible factor-1alpha protein synthesis. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 94-97 25383959-0 2014 Celastrol stimulates hypoxia-inducible factor-1 activity in tumor cells by initiating the ROS/Akt/p70S6K signaling pathway and enhancing hypoxia-inducible factor-1alpha protein synthesis. celastrol 0-9 ribosomal protein S6 kinase B1 Homo sapiens 98-104 25383959-0 2014 Celastrol stimulates hypoxia-inducible factor-1 activity in tumor cells by initiating the ROS/Akt/p70S6K signaling pathway and enhancing hypoxia-inducible factor-1alpha protein synthesis. celastrol 0-9 hypoxia inducible factor 1 subunit alpha Homo sapiens 137-168 25383959-3 2014 In this study, we reported for the first time that Celastrol could induce HIF-1alpha protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1alpha protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. celastrol 51-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 74-84 25383959-3 2014 In this study, we reported for the first time that Celastrol could induce HIF-1alpha protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1alpha protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. celastrol 51-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 74-79 25383959-3 2014 In this study, we reported for the first time that Celastrol could induce HIF-1alpha protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1alpha protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. celastrol 51-60 vascular endothelial growth factor A Homo sapiens 286-290 25383959-3 2014 In this study, we reported for the first time that Celastrol could induce HIF-1alpha protein accumulation in multiple cancer cell lines in an oxygen-independent manner and that the enhanced HIF-1alpha protein entered the nucleus and promoted the transcription of the HIF-1 target genes VEGF and Glut-1. celastrol 51-60 solute carrier family 2 member 1 Homo sapiens 295-301 25383959-5 2014 Instead, Celastrol induced the accumulation of the HIF-1alpha protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1alpha translation. celastrol 9-18 hypoxia inducible factor 1 subunit alpha Homo sapiens 51-61 25383959-5 2014 Instead, Celastrol induced the accumulation of the HIF-1alpha protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1alpha translation. celastrol 9-18 AKT serine/threonine kinase 1 Homo sapiens 101-104 25383959-5 2014 Instead, Celastrol induced the accumulation of the HIF-1alpha protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1alpha translation. celastrol 9-18 ribosomal protein S6 kinase B1 Homo sapiens 105-111 25383959-5 2014 Instead, Celastrol induced the accumulation of the HIF-1alpha protein by inducing ROS and activating Akt/p70S6K signaling to promote HIF-1alpha translation. celastrol 9-18 hypoxia inducible factor 1 subunit alpha Homo sapiens 133-143 25383959-6 2014 In addition, we found that the activation of Akt by Celastrol was transient. celastrol 52-61 AKT serine/threonine kinase 1 Homo sapiens 45-48 25383959-7 2014 With increased exposure time, inhibition of Hsp90 chaperone function by Celastrol led to the subsequent depletion of the Akt protein and thus to the suppression of Akt activity. celastrol 72-81 AKT serine/threonine kinase 1 Homo sapiens 121-124 25383959-7 2014 With increased exposure time, inhibition of Hsp90 chaperone function by Celastrol led to the subsequent depletion of the Akt protein and thus to the suppression of Akt activity. celastrol 72-81 AKT serine/threonine kinase 1 Homo sapiens 164-167 25383959-10 2014 Furthermore, our data showed that the dose required for Celastrol to induce HIF-1alpha protein accumulation and enhance HIF-1alpha transcriptional activation was below its cytotoxic threshold. celastrol 56-65 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-86 25383959-11 2014 A cytotoxic dose of Celastrol for cancer cells did not display cytotoxicity in LO2 normal human liver cells, which indicated that the novel functions of Celastrol in regulating HIF-1 signaling and inducing autophagy might be used in new applications, such as in anti-inflammation and protection of cells against human neurodegenerative diseases. celastrol 20-29 hypoxia inducible factor 1 subunit alpha Homo sapiens 177-182 25383959-11 2014 A cytotoxic dose of Celastrol for cancer cells did not display cytotoxicity in LO2 normal human liver cells, which indicated that the novel functions of Celastrol in regulating HIF-1 signaling and inducing autophagy might be used in new applications, such as in anti-inflammation and protection of cells against human neurodegenerative diseases. celastrol 153-162 hypoxia inducible factor 1 subunit alpha Homo sapiens 177-182 25218987-8 2014 Moreover, celastrol treatment resulted in significant reduction in NF-kappaB expression, nitrites levels, as well as immunohistochemical expression of TLR2 and CD3+ T-lymphocytic count. celastrol 10-19 toll-like receptor 2 Rattus norvegicus 151-155 24615207-0 2014 Simultaneous NF-kappaB inhibition and E-cadherin upregulation mediate mutually synergistic anticancer activity of celastrol and SAHA in vitro and in vivo. celastrol 114-123 cadherin 1 Homo sapiens 38-48 24615207-5 2014 Interestingly, E-cadherin was dramatically downregulated in celastrol-resistant cancer cells, and E-cadherin expression was closely related to decreased sensitivity to celastrol. celastrol 60-69 cadherin 1 Homo sapiens 15-25 24615207-5 2014 Interestingly, E-cadherin was dramatically downregulated in celastrol-resistant cancer cells, and E-cadherin expression was closely related to decreased sensitivity to celastrol. celastrol 168-177 cadherin 1 Homo sapiens 98-108 24615207-8 2014 Taken together, our data demonstrated the synergistic anticancer effects of celastrol and SAHA due to their reciprocal sensitisation, which was simultaneously regulated by NF-kappaB and E-cadherin; thus, the combination of celastrol and SAHA was superior to other combination regimens that rely on a single mechanism. celastrol 76-85 cadherin 1 Homo sapiens 186-196 25064159-7 2014 Furthermore, celastrol induced mRNA and protein expression of HO-1 as well as Nrf2 activation. celastrol 13-22 NFE2 like bZIP transcription factor 2 Homo sapiens 78-82 25149175-0 2014 Release of Ca2+ from the endoplasmic reticulum and its subsequent influx into mitochondria trigger celastrol-induced paraptosis in cancer cells. celastrol 99-108 carbonic anhydrase 2 Homo sapiens 11-14 25149175-3 2014 Celastrol treatment markedly increased mitochondrial Ca2+ levels and induced ER stress via proteasome inhibition in these cells. celastrol 0-9 carbonic anhydrase 2 Homo sapiens 53-56 25149175-4 2014 Both MCU (mitochondrial Ca2+ uniporter) knockdown and pretreatment with ruthenium red, an inhibitor of MCU, inhibited celastrol-induced mitochondrial Ca2+ uptake, dilation of mitochondria/ER, accumulation of poly-ubiquitinated proteins, and cell death in MDA-MB 435S cells. celastrol 118-127 mitochondrial calcium uniporter Homo sapiens 5-8 25149175-4 2014 Both MCU (mitochondrial Ca2+ uniporter) knockdown and pretreatment with ruthenium red, an inhibitor of MCU, inhibited celastrol-induced mitochondrial Ca2+ uptake, dilation of mitochondria/ER, accumulation of poly-ubiquitinated proteins, and cell death in MDA-MB 435S cells. celastrol 118-127 mitochondrial calcium uniporter Homo sapiens 10-38 25149175-4 2014 Both MCU (mitochondrial Ca2+ uniporter) knockdown and pretreatment with ruthenium red, an inhibitor of MCU, inhibited celastrol-induced mitochondrial Ca2+ uptake, dilation of mitochondria/ER, accumulation of poly-ubiquitinated proteins, and cell death in MDA-MB 435S cells. celastrol 118-127 mitochondrial calcium uniporter Homo sapiens 103-106 25149175-4 2014 Both MCU (mitochondrial Ca2+ uniporter) knockdown and pretreatment with ruthenium red, an inhibitor of MCU, inhibited celastrol-induced mitochondrial Ca2+ uptake, dilation of mitochondria/ER, accumulation of poly-ubiquitinated proteins, and cell death in MDA-MB 435S cells. celastrol 118-127 carbonic anhydrase 2 Homo sapiens 24-27 24700193-1 2014 Hsp70, Hsp32, and Hsp27 were induced by celastrol in rat cerebral cortical cultures at dosages that did not affect cell viability. celastrol 40-49 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 0-5 24700193-1 2014 Hsp70, Hsp32, and Hsp27 were induced by celastrol in rat cerebral cortical cultures at dosages that did not affect cell viability. celastrol 40-49 heme oxygenase 1 Rattus norvegicus 7-12 24700193-1 2014 Hsp70, Hsp32, and Hsp27 were induced by celastrol in rat cerebral cortical cultures at dosages that did not affect cell viability. celastrol 40-49 heat shock protein family B (small) member 1 Rattus norvegicus 18-23 24700193-3 2014 Celastrol-induced Hsp70 localized to the cell body and cellular processes of neurons that were identified by neuron-specific betaIII-tubulin. celastrol 0-9 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 18-23 25138213-3 2014 Celastrol and Taxol decreased the expression of HDAC3 in cancer cell lines sensitive to anti-cancer drugs. celastrol 0-9 histone deacetylase 3 Homo sapiens 48-53 24954307-0 2014 The effect of celastrol, a triterpene with antitumorigenic activity, on conformational and functional aspects of the human 90kDa heat shock protein Hsp90alpha, a chaperone implicated in the stabilization of the tumor phenotype. celastrol 14-23 heat shock protein 90 alpha family class A member 1 Homo sapiens 148-158 24954307-3 2014 RESULTS: In this work, we investigated the effect of celastrol on the conformational and functional aspects of Hsp90alpha. celastrol 53-62 heat shock protein 90 alpha family class A member 1 Homo sapiens 111-121 24954307-4 2014 Interestingly, celastrol appeared to target Hsp90alpha directly as the compound induced the oligomerization of the chaperone via the C-terminal domain as demonstrated by experiments using a deletion mutant. celastrol 15-24 heat shock protein 90 alpha family class A member 1 Homo sapiens 44-54 24954307-5 2014 The nature of the oligomers was investigated by biophysical tools demonstrating that a two-fold excess of celastrol induced the formation of a decameric Hsp90alpha bound throughout the C-terminal domain. celastrol 106-115 heat shock protein 90 alpha family class A member 1 Homo sapiens 153-163 24954307-8 2014 CONCLUSION: Celastrol interferes with specific biological functions of Hsp90alpha. celastrol 12-21 heat shock protein 90 alpha family class A member 1 Homo sapiens 71-81 24954307-9 2014 Our results suggest a model in which celastrol binds directly to the C-terminal domain of Hsp90alpha causing oligomerization. celastrol 37-46 heat shock protein 90 alpha family class A member 1 Homo sapiens 90-100 24954307-11 2014 Therefore celastrol may act primarily by inducing specific oligomerization that affects some, but not all, of the functions of Hsp90alpha. celastrol 10-19 heat shock protein 90 alpha family class A member 1 Homo sapiens 127-137 24954307-12 2014 GENERAL SIGNIFICANCE: To the best of our knowledge, this study is the first work to use multiple probes to investigate the effect that celastrol has on the stability and oligomerization of Hsp90alpha and on the binding of this chaperone to Tom70. celastrol 135-144 heat shock protein 90 alpha family class A member 1 Homo sapiens 189-199 24954307-12 2014 GENERAL SIGNIFICANCE: To the best of our knowledge, this study is the first work to use multiple probes to investigate the effect that celastrol has on the stability and oligomerization of Hsp90alpha and on the binding of this chaperone to Tom70. celastrol 135-144 translocase of outer mitochondrial membrane 70 Homo sapiens 240-245 24954307-13 2014 This work provides a novel mechanism by which celastrol binds Hsp90alpha. celastrol 46-55 heat shock protein 90 alpha family class A member 1 Homo sapiens 62-72 24903326-12 2014 In addition, (b) using drugs (Celastrol or BGP-15) to increase Hsp70/Hsp110 levels protect cells against TBI, suggesting the beneficial effects of Hsp70/Hsp110 inducers to reduce the pathological consequences of TBI. celastrol 30-39 heat shock protein 1B Mus musculus 63-68 24903326-12 2014 In addition, (b) using drugs (Celastrol or BGP-15) to increase Hsp70/Hsp110 levels protect cells against TBI, suggesting the beneficial effects of Hsp70/Hsp110 inducers to reduce the pathological consequences of TBI. celastrol 30-39 heat shock 105kDa/110kDa protein 1 Mus musculus 69-75 24903326-12 2014 In addition, (b) using drugs (Celastrol or BGP-15) to increase Hsp70/Hsp110 levels protect cells against TBI, suggesting the beneficial effects of Hsp70/Hsp110 inducers to reduce the pathological consequences of TBI. celastrol 30-39 heat shock protein 1B Mus musculus 147-152 24903326-12 2014 In addition, (b) using drugs (Celastrol or BGP-15) to increase Hsp70/Hsp110 levels protect cells against TBI, suggesting the beneficial effects of Hsp70/Hsp110 inducers to reduce the pathological consequences of TBI. celastrol 30-39 heat shock 105kDa/110kDa protein 1 Mus musculus 153-159 25149175-5 2014 Inhibition of the IP3 receptor (IP3R) with 2-aminoethoxydiphenyl borate (2-APB) also effectively blocked celastrol-induced mitochondrial Ca2+ accumulation and subsequent paraptotic events. celastrol 105-114 inositol 1,4,5-trisphosphate receptor type 3 Homo sapiens 32-36 25149175-5 2014 Inhibition of the IP3 receptor (IP3R) with 2-aminoethoxydiphenyl borate (2-APB) also effectively blocked celastrol-induced mitochondrial Ca2+ accumulation and subsequent paraptotic events. celastrol 105-114 carbonic anhydrase 2 Homo sapiens 137-140 25149175-6 2014 Collectively, our results show that the IP3R-mediated release of Ca2+ from the ER and its subsequent MCU-mediatedinflux into mitochondria critically contribute to celastrol-induced paraptosis in cancer cells. celastrol 163-172 inositol 1,4,5-trisphosphate receptor type 3 Homo sapiens 40-44 25149175-6 2014 Collectively, our results show that the IP3R-mediated release of Ca2+ from the ER and its subsequent MCU-mediatedinflux into mitochondria critically contribute to celastrol-induced paraptosis in cancer cells. celastrol 163-172 carbonic anhydrase 2 Homo sapiens 65-68 25149175-6 2014 Collectively, our results show that the IP3R-mediated release of Ca2+ from the ER and its subsequent MCU-mediatedinflux into mitochondria critically contribute to celastrol-induced paraptosis in cancer cells. celastrol 163-172 mitochondrial calcium uniporter Homo sapiens 101-104 25116125-0 2014 Celastrol inhibits lung infiltration in differential syndrome animal models by reducing TNF-alpha and ICAM-1 levels while preserving differentiation in ATRA-induced acute promyelocytic leukemia cells. celastrol 0-9 tumor necrosis factor Homo sapiens 88-97 25116125-0 2014 Celastrol inhibits lung infiltration in differential syndrome animal models by reducing TNF-alpha and ICAM-1 levels while preserving differentiation in ATRA-induced acute promyelocytic leukemia cells. celastrol 0-9 intercellular adhesion molecule 1 Homo sapiens 102-108 25116125-5 2014 In ATRA-treated NB4 cells, celastrol could potently inhibit ICAM-1 elevation and partially reduce TNF-alpha and IL-1beta secretion, though treatment showed no effects on IL-8 and MCP-1 levels. celastrol 27-36 intercellular adhesion molecule 1 Homo sapiens 60-66 25116125-5 2014 In ATRA-treated NB4 cells, celastrol could potently inhibit ICAM-1 elevation and partially reduce TNF-alpha and IL-1beta secretion, though treatment showed no effects on IL-8 and MCP-1 levels. celastrol 27-36 tumor necrosis factor Homo sapiens 98-107 25116125-5 2014 In ATRA-treated NB4 cells, celastrol could potently inhibit ICAM-1 elevation and partially reduce TNF-alpha and IL-1beta secretion, though treatment showed no effects on IL-8 and MCP-1 levels. celastrol 27-36 interleukin 1 beta Homo sapiens 112-120 25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. celastrol 0-9 intercellular adhesion molecule 1 Homo sapiens 22-28 25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. celastrol 0-9 mitogen-activated protein kinase kinase 1 Homo sapiens 73-77 25116125-6 2014 Celastrol"s effect on ICAM-1 in ATRA-treated NB4 was related to reducing MEK1/ERK1 activation. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 78-82 25101848-13 2014 Taken together, our results demonstrate the analgesia effects of celastrol through CB2 signaling and propose the potential of exploiting celastrol as a novel candidate for pain relief. celastrol 65-74 cannabinoid receptor 2 (macrophage) Mus musculus 83-86 25076938-15 2014 Furthermore, celastrol suppressed TGF-beta1 induced EMT in thyroid cancer cells and may have therapeutic potential. celastrol 13-22 transforming growth factor, beta 1 Mus musculus 34-43 24859482-0 2014 Celastrol inhibits the HIF-1alpha pathway by inhibition of mTOR/p70S6K/eIF4E and ERK1/2 phosphorylation in human hepatoma cells. celastrol 0-9 hypoxia inducible factor 1 subunit alpha Homo sapiens 23-33 25126165-7 2014 The expression of VEGF in the celastrol group was significantly less compared with the model group (P = 0.014), whereas the expression of VEGF in the atorvastatin group and the model group showed no significant differences. celastrol 30-39 vascular endothelial growth factor A Oryctolagus cuniculus 18-22 25126165-8 2014 CONCLUSION: Our findings suggest that celastrol effectively reduced the plaque ratio, decreased the serum levels of LDL and downregulated the expression of VEGF, suggesting an anti-AS effect of celastrol. celastrol 38-47 vascular endothelial growth factor A Oryctolagus cuniculus 156-160 25126165-8 2014 CONCLUSION: Our findings suggest that celastrol effectively reduced the plaque ratio, decreased the serum levels of LDL and downregulated the expression of VEGF, suggesting an anti-AS effect of celastrol. celastrol 194-203 vascular endothelial growth factor A Oryctolagus cuniculus 156-160 24859482-0 2014 Celastrol inhibits the HIF-1alpha pathway by inhibition of mTOR/p70S6K/eIF4E and ERK1/2 phosphorylation in human hepatoma cells. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 59-63 24859482-0 2014 Celastrol inhibits the HIF-1alpha pathway by inhibition of mTOR/p70S6K/eIF4E and ERK1/2 phosphorylation in human hepatoma cells. celastrol 0-9 ribosomal protein S6 kinase B1 Homo sapiens 64-70 24859482-0 2014 Celastrol inhibits the HIF-1alpha pathway by inhibition of mTOR/p70S6K/eIF4E and ERK1/2 phosphorylation in human hepatoma cells. celastrol 0-9 eukaryotic translation initiation factor 4E Homo sapiens 71-76 24859482-0 2014 Celastrol inhibits the HIF-1alpha pathway by inhibition of mTOR/p70S6K/eIF4E and ERK1/2 phosphorylation in human hepatoma cells. celastrol 0-9 mitogen-activated protein kinase 3 Homo sapiens 81-87 24859482-2 2014 In a search for HIF-1 inhibitors, we identified celastrol as an inhibitor of HIF-1 activation from Tripterygium wilfordii. celastrol 48-57 hypoxia inducible factor 1 subunit alpha Homo sapiens 16-21 24859482-2 2014 In a search for HIF-1 inhibitors, we identified celastrol as an inhibitor of HIF-1 activation from Tripterygium wilfordii. celastrol 48-57 hypoxia inducible factor 1 subunit alpha Homo sapiens 77-82 24859482-3 2014 In the present study, we demonstrated the effect of celastrol on HIF-1 activation. celastrol 52-61 hypoxia inducible factor 1 subunit alpha Homo sapiens 65-70 24859482-4 2014 Celastrol showed a potent inhibitory activity against HIF-1 activation induced by hypoxia in various human cancer cell lines. celastrol 0-9 hypoxia inducible factor 1 subunit alpha Homo sapiens 54-59 24859482-6 2014 Furthermore, celastrol prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). celastrol 13-22 hypoxia inducible factor 1 subunit alpha Homo sapiens 63-68 24859482-6 2014 Furthermore, celastrol prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). celastrol 13-22 vascular endothelial growth factor A Homo sapiens 86-120 24859482-6 2014 Furthermore, celastrol prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). celastrol 13-22 vascular endothelial growth factor A Homo sapiens 122-126 24859482-6 2014 Furthermore, celastrol prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). celastrol 13-22 erythropoietin Homo sapiens 132-146 24859482-6 2014 Furthermore, celastrol prevented hypoxia-induced expression of HIF-1 target genes for vascular endothelial growth factor (VEGF) and erythropoietin (EPO). celastrol 13-22 erythropoietin Homo sapiens 148-151 24859482-7 2014 Further analysis revealed that celastrol inhibited HIF-1alpha protein synthesis, without affecting the expression level of HIF-1alpha mRNA or degradation of HIF-1alpha protein. celastrol 31-40 hypoxia inducible factor 1 subunit alpha Homo sapiens 51-61 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 39-49 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 mechanistic target of rapamycin kinase Homo sapiens 120-149 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 mechanistic target of rapamycin kinase Homo sapiens 151-155 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 ribosomal protein S6 kinase B1 Homo sapiens 205-211 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 eukaryotic translation initiation factor 4E Homo sapiens 217-248 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 eukaryotic translation initiation factor 4E Homo sapiens 250-255 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 mitogen-activated protein kinase 1 Homo sapiens 261-298 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 mitogen-activated protein kinase 1 Homo sapiens 300-303 24859482-8 2014 Markedly, we found that suppression of HIF-1alpha accumulation by celastrol correlated with strong dephosphorylation of mammalian target of rapamycin (mTOR) and its effectors, ribosomal protein S6 kinase (p70S6K) and eukaryotic initiation factor 4E (eIF4E) and extracellular signal-regulated kinase (ERK), pathways known to regulate HIF-1alpha expression at the translational level. celastrol 66-75 hypoxia inducible factor 1 subunit alpha Homo sapiens 333-343 24859482-9 2014 In vivo studies further confirmed the inhibitory effect of celastrol on the expression of HIF-1alpha proteins, leading to a decreased growth of Hep3B cells in a xenograft tumor model. celastrol 59-68 hypoxia inducible factor 1 subunit alpha Homo sapiens 90-100 24859482-10 2014 Our data suggested that celastrol is an effective inhibitor of HIF-1 and provide new perspectives into the mechanism of its anticancer activity. celastrol 24-33 hypoxia inducible factor 1 subunit alpha Homo sapiens 63-68 24849358-7 2014 In vivo celastrol increased the HSF1 ChIP signal in hippocampus but not in liver. celastrol 8-17 heat shock transcription factor 1 Homo sapiens 32-36 24927548-2 2014 Two of the 50 predicted hits had activity against either human FPPS (HsFPPS) or Trypanosoma brucei FPPS (TbFPPS), the most active being the quinone methide celastrol (IC50 versus TbFPPS ~ 20 microM). celastrol 156-165 farnesyl diphosphate synthase Homo sapiens 63-67 24810052-5 2014 Our studies indicate that celastrol promotes proteotoxic stress, supported by two feedback mechanisms: (i) impairment of protein quality control as revealed by accumulation of polyubiquitinated aggregates and the canonical autophagy substrate, p62, and (ii) the induction of heat-shock proteins, HSP72 and HSP90. celastrol 26-35 nucleoporin 62 Homo sapiens 244-247 24810052-5 2014 Our studies indicate that celastrol promotes proteotoxic stress, supported by two feedback mechanisms: (i) impairment of protein quality control as revealed by accumulation of polyubiquitinated aggregates and the canonical autophagy substrate, p62, and (ii) the induction of heat-shock proteins, HSP72 and HSP90. celastrol 26-35 heat shock protein family A (Hsp70) member 1A Homo sapiens 296-301 24810052-5 2014 Our studies indicate that celastrol promotes proteotoxic stress, supported by two feedback mechanisms: (i) impairment of protein quality control as revealed by accumulation of polyubiquitinated aggregates and the canonical autophagy substrate, p62, and (ii) the induction of heat-shock proteins, HSP72 and HSP90. celastrol 26-35 heat shock protein 90 alpha family class A member 1 Homo sapiens 306-311 24810052-9 2014 This study further emphasizes that targeting proteotoxic stress responses by inhibiting HSP90 with 17-N-Allylamino-17-demethoxygeldanamycin sensitizes human glioblastoma to celastrol treatment, thereby serving as a novel synergism to overcome drug resistance. celastrol 173-182 heat shock protein 90 alpha family class A member 1 Homo sapiens 88-93 24293411-0 2014 Cancerous inhibitor of PP2A is targeted by natural compound celastrol for degradation in non-small-cell lung cancer. celastrol 60-69 cellular inhibitor of PP2A Homo sapiens 0-27 24755677-0 2014 NF-kappa B modulation is involved in celastrol induced human multiple myeloma cell apoptosis. celastrol 37-46 nuclear factor kappa B subunit 1 Homo sapiens 0-10 24755677-5 2014 Celastrol inhibited cell proliferation of LP-1 myeloma cell in a dose-dependent manner with IC50 values of 0.8817 microM, which was mediated through G1 cell cycle arrest and p27 induction. celastrol 0-9 dynactin subunit 6 Homo sapiens 174-177 24755677-6 2014 Celastrol induced apoptosis in LP-1 and RPMI 8226 myeloma cells in a time and dose dependent manner, and it involved Caspase-3 activation and NF-kappaB pathway. celastrol 0-9 caspase 3 Homo sapiens 117-126 24755677-6 2014 Celastrol induced apoptosis in LP-1 and RPMI 8226 myeloma cells in a time and dose dependent manner, and it involved Caspase-3 activation and NF-kappaB pathway. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 142-151 24755677-7 2014 Celastrol down-modulated antiapoptotic proteins including Bcl-2 and survivin expression. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 58-63 24755677-8 2014 The expression of NF-kappaB and IKKa were decreased after celastrol treatment. celastrol 58-67 nuclear factor kappa B subunit 1 Homo sapiens 18-27 24755677-8 2014 The expression of NF-kappaB and IKKa were decreased after celastrol treatment. celastrol 58-67 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 32-36 24755677-9 2014 Celastrol effectively blocked the nuclear translocation of the p65 subunit and induced human multiple myeloma cell cycle arrest and apoptosis by p27 upregulation and NF-kB modulation. celastrol 0-9 RELA proto-oncogene, NF-kB subunit Homo sapiens 63-66 24755677-9 2014 Celastrol effectively blocked the nuclear translocation of the p65 subunit and induced human multiple myeloma cell cycle arrest and apoptosis by p27 upregulation and NF-kB modulation. celastrol 0-9 dynactin subunit 6 Homo sapiens 145-148 24293411-1 2014 Celastrol binds CIP2A and enhances CIP2A-CHIP interaction, leading to ubiquitination/degradation of CIP2A and inhibition of lung cancer cells in vitro and in vivo. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 16-21 24293411-1 2014 Celastrol binds CIP2A and enhances CIP2A-CHIP interaction, leading to ubiquitination/degradation of CIP2A and inhibition of lung cancer cells in vitro and in vivo. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 35-40 24293411-1 2014 Celastrol binds CIP2A and enhances CIP2A-CHIP interaction, leading to ubiquitination/degradation of CIP2A and inhibition of lung cancer cells in vitro and in vivo. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 35-40 24293411-2 2014 Celastrol potentiates cisplatin"s efficacy by suppressing the CIP2A-Akt pathway, and therefore CIP2A inhibitors may represent novel therapeutics for cancer. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 62-71 24293411-2 2014 Celastrol potentiates cisplatin"s efficacy by suppressing the CIP2A-Akt pathway, and therefore CIP2A inhibitors may represent novel therapeutics for cancer. celastrol 0-9 cellular inhibitor of PP2A Homo sapiens 62-67 24664372-5 2014 Knockdown of IL-6 attenuated the anti-proliferative effect of celastrol on PC-3 cells. celastrol 62-71 interleukin 6 Homo sapiens 13-17 24265268-5 2014 In a cell-free environment, IP-FCM could detect the direct effects of ATP and/or HSP90 inhibitors (17-N-allylamino-17-demethoxygeldanamycin or celastrol) in causing component dissociation and the time- and dose-effects of inhibitor-caused dissociation. celastrol 143-152 heat shock protein 90 alpha family class A member 1 Homo sapiens 81-86 24965400-8 2014 Moreover, celastrol enhanced the ability of lapatinib to down regulate EGFR protein expression in HepG2 cells. celastrol 10-19 epidermal growth factor receptor Homo sapiens 71-75 25007672-9 2014 The potential mechanism may be related to the upregulation of NRF2 nuclear protein expression and GCLC cytoplasmic expression after celastrol pretreatment. celastrol 132-141 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 98-102 24664372-0 2014 Celastrol blocks interleukin-6 gene expression via downregulation of NF-kappaB in prostate carcinoma cells. celastrol 0-9 interleukin 6 Homo sapiens 17-30 24664372-0 2014 Celastrol blocks interleukin-6 gene expression via downregulation of NF-kappaB in prostate carcinoma cells. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 69-78 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 83-92 interleukin 6 Homo sapiens 113-117 24664372-3 2014 In this study, we evaluated the molecular mechanisms of celastrol on cell proliferation and IL-6 gene expression in prostate carcinoma cells. celastrol 56-65 interleukin 6 Homo sapiens 92-96 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 83-92 nuclear factor kappa B subunit 1 Homo sapiens 185-194 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 83-92 interleukin 6 Homo sapiens 219-223 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 83-92 nuclear factor kappa B subunit 1 Homo sapiens 260-269 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 83-92 interleukin 6 Homo sapiens 219-223 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 388-397 interleukin 6 Homo sapiens 219-223 24664372-6 2014 Results from ELISA and 5"-deletion transient gene expression assays indicated that celastrol treatment decreased IL-6 secretion and gene expression, and this effect is dependent on the NF-kappaB response element within IL-6 promoter area since mutation of the NF-kappaB response element from AAATGTCCCATTTTCCC to AAATGTTACATTTTCCC by site-directed mutagenesis abolished the inhibition of celastrol on the IL-6 promoter activity. celastrol 388-397 interleukin 6 Homo sapiens 219-223 24664372-7 2014 Celastrol also attenuated the activation of PMA and TNFalpha on the gene expression and secretion of IL-6 in PC-3 cells. celastrol 0-9 tumor necrosis factor Homo sapiens 52-60 24664372-7 2014 Celastrol also attenuated the activation of PMA and TNFalpha on the gene expression and secretion of IL-6 in PC-3 cells. celastrol 0-9 interleukin 6 Homo sapiens 101-105 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 32-41 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 85-93 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 32-41 nuclear factor kappa B subunit 1 Homo sapiens 95-98 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 32-41 RELA proto-oncogene, NF-kB subunit Homo sapiens 103-106 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 32-41 interleukin 6 Homo sapiens 197-201 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 32-41 nuclear factor kappa B subunit 1 Homo sapiens 225-234 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 179-188 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 85-93 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 179-188 nuclear factor kappa B subunit 1 Homo sapiens 95-98 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 179-188 RELA proto-oncogene, NF-kB subunit Homo sapiens 103-106 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 179-188 interleukin 6 Homo sapiens 197-201 24664372-8 2014 Immunoblot assays revealed that celastrol treatment downregulated the expressions of IKKalpha, p50 and p65, supporting the 5"-deletion transient gene expression assay result that celastrol blocked IL-6 expression through the NF-kappaB pathway in PC-3 cells. celastrol 179-188 nuclear factor kappa B subunit 1 Homo sapiens 225-234 24664372-9 2014 For the first time, our results concluded that celastrol attenuates PC-3 cell proliferation via downregulation of IL-6 gene expression through the NF-kappaB-dependent pathway. celastrol 47-56 interleukin 6 Homo sapiens 114-118 24664372-9 2014 For the first time, our results concluded that celastrol attenuates PC-3 cell proliferation via downregulation of IL-6 gene expression through the NF-kappaB-dependent pathway. celastrol 47-56 nuclear factor kappa B subunit 1 Homo sapiens 147-156 24384223-2 2014 Here, we investigated the effect of the novel NF-kappaB inhibitor celastrol on murine colitis. celastrol 66-75 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 46-55 24589236-0 2014 Peptide deformylase inhibitor actinonin reduces celastrol"s HSP70 induction while synergizing proliferation inhibition in tumor cells. celastrol 48-57 heat shock protein family A (Hsp70) member 4 Homo sapiens 60-65 24589236-1 2014 BACKGROUND: Celastrol is a promising anti-tumor agent, yet it also elevates heat shock proteins (HSPs), especially HSP70, this effect believed to reduce its anti-tumor effects. celastrol 12-21 heat shock protein family A (Hsp70) member 4 Homo sapiens 115-120 24589236-2 2014 Concurrent use of siRNA to increase celastrol"s anti-tumor effects through HSP70 interference has been reported, but because siRNA technology is difficult to clinically apply, an alternative way to curb unwanted HSP70 elevation caused by celastrol treatment is worth exploring. celastrol 36-45 heat shock protein family A (Hsp70) member 4 Homo sapiens 75-80 24589236-2 2014 Concurrent use of siRNA to increase celastrol"s anti-tumor effects through HSP70 interference has been reported, but because siRNA technology is difficult to clinically apply, an alternative way to curb unwanted HSP70 elevation caused by celastrol treatment is worth exploring. celastrol 238-247 heat shock protein family A (Hsp70) member 4 Homo sapiens 212-217 24589236-4 2014 RESULTS: The first strategy was unsuccessful since celastrol treatment increased HSP70 in all 7 of the cancer cell types tested, this result related to HSF1 activation. celastrol 51-60 heat shock protein family A (Hsp70) member 4 Homo sapiens 81-86 24589236-4 2014 RESULTS: The first strategy was unsuccessful since celastrol treatment increased HSP70 in all 7 of the cancer cell types tested, this result related to HSF1 activation. celastrol 51-60 heat shock transcription factor 1 Homo sapiens 152-156 24589236-5 2014 The ubiquity of HSF1 expression in different cancer cells might explain why celastrol has no cell-type limitation for HSP70 induction. celastrol 76-85 heat shock transcription factor 1 Homo sapiens 16-20 24589236-6 2014 The second strategy revealed that modification of celastrol"s carboxyl group abolished its ability to elevate HSP70, but also abolished celastrol"s tumor inhibition effects. celastrol 50-59 heat shock protein family A (Hsp70) member 4 Homo sapiens 110-115 24589236-7 2014 In the third strategy, 11 inhibitors for 10 signaling proteins reportedly related to celastrol action were tested, and five of these could reduce celastrol-caused HSP70 elevation. celastrol 146-155 heat shock protein family A (Hsp70) member 4 Homo sapiens 163-168 24589236-9 2014 CONCLUSIONS: Concurrent use of the chemical agent actinonin could reduce celastrol"s HSP70 elevation and also enhance proliferation inhibition by celastrol. celastrol 73-82 heat shock protein family A (Hsp70) member 4 Homo sapiens 85-90 24465597-6 2014 RESULTS: Celastrol, resveratrol, sulphoraphane and curcumin inhibited the NF-kappaB promoter activity significantly and in a dose dependent manner. celastrol 9-18 nuclear factor kappa B subunit 1 Homo sapiens 74-83 24157922-11 2014 VEGF levels decreased by 64.8, 84.4 and 92.9% after coexposure to celastrol at 0.025, 0.05 and 0.1 muM, respectively, compared to LPS alone. celastrol 66-75 vascular endothelial growth factor A Homo sapiens 0-4 24351928-4 2014 Celastrol interfered with the establishment of the heat-shock protein 90/Hsp90 cochaperone Cdc37/Hsp90-Hsp70-organizing protein chaperone complex with mutant GCase and reduced heat-shock protein 90-associated protein degradation. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 73-78 24351928-4 2014 Celastrol interfered with the establishment of the heat-shock protein 90/Hsp90 cochaperone Cdc37/Hsp90-Hsp70-organizing protein chaperone complex with mutant GCase and reduced heat-shock protein 90-associated protein degradation. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 91-96 24351928-4 2014 Celastrol interfered with the establishment of the heat-shock protein 90/Hsp90 cochaperone Cdc37/Hsp90-Hsp70-organizing protein chaperone complex with mutant GCase and reduced heat-shock protein 90-associated protein degradation. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 97-102 24351928-4 2014 Celastrol interfered with the establishment of the heat-shock protein 90/Hsp90 cochaperone Cdc37/Hsp90-Hsp70-organizing protein chaperone complex with mutant GCase and reduced heat-shock protein 90-associated protein degradation. celastrol 0-9 heat shock protein family A (Hsp70) member 4 Homo sapiens 103-108 24351928-6 2014 Bcl2-associated athanogene 3 and heat shock 70kDa proteins 1A and 1B were significantly increased by celastrol. celastrol 101-110 BAG cochaperone 3 Homo sapiens 0-28 24157922-0 2014 Celastrol inhibits lipopolysaccharide-induced angiogenesis by suppressing TLR4-triggered nuclear factor-kappa B activation. celastrol 0-9 toll like receptor 4 Homo sapiens 74-78 24157922-0 2014 Celastrol inhibits lipopolysaccharide-induced angiogenesis by suppressing TLR4-triggered nuclear factor-kappa B activation. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 89-111 24157922-9 2014 A 45-74% inhibition of LPS-dependent cell invasion was achieved in the presence of 0.025-0.1 muM celastrol. celastrol 97-106 latexin Homo sapiens 93-96 24157922-10 2014 Celastrol significantly downregulated LPS-induced TLR4 expression and inhibited LPS-induced VEGF secretion in LP-1 cells. celastrol 0-9 toll like receptor 4 Homo sapiens 50-54 24157922-10 2014 Celastrol significantly downregulated LPS-induced TLR4 expression and inhibited LPS-induced VEGF secretion in LP-1 cells. celastrol 0-9 vascular endothelial growth factor A Homo sapiens 92-96 24157922-11 2014 VEGF levels decreased by 64.8, 84.4 and 92.9% after coexposure to celastrol at 0.025, 0.05 and 0.1 muM, respectively, compared to LPS alone. celastrol 66-75 latexin Homo sapiens 99-102 24157922-12 2014 Celastrol also inhibited the IkappaB kinase (IKK)/NF-kappaB pathway induced by LPS. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 50-59 24157922-13 2014 Protein levels of NF-kappaB p65, IKKalpha and IkappaB-alpha decreased in a dose-dependent manner after coexposure to celastrol. celastrol 117-126 nuclear factor kappa B subunit 1 Homo sapiens 18-27 24157922-13 2014 Protein levels of NF-kappaB p65, IKKalpha and IkappaB-alpha decreased in a dose-dependent manner after coexposure to celastrol. celastrol 117-126 RELA proto-oncogene, NF-kB subunit Homo sapiens 28-31 24157922-13 2014 Protein levels of NF-kappaB p65, IKKalpha and IkappaB-alpha decreased in a dose-dependent manner after coexposure to celastrol. celastrol 117-126 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 33-41 24157922-13 2014 Protein levels of NF-kappaB p65, IKKalpha and IkappaB-alpha decreased in a dose-dependent manner after coexposure to celastrol. celastrol 117-126 NFKB inhibitor alpha Homo sapiens 46-59 24157922-14 2014 Celastrol also blocked nuclear translocation of the p65 subunit. celastrol 0-9 RELA proto-oncogene, NF-kB subunit Homo sapiens 52-55 24157922-15 2014 These results suggest that celastrol inhibits LPS-induced angiogenesis by suppressing TLR4-triggered NF-kappaB activation. celastrol 27-36 toll like receptor 4 Homo sapiens 86-90 24157922-15 2014 These results suggest that celastrol inhibits LPS-induced angiogenesis by suppressing TLR4-triggered NF-kappaB activation. celastrol 27-36 nuclear factor kappa B subunit 1 Homo sapiens 101-110 24111524-10 2014 The findings indicate that celastrol prevents Cd-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 27-36 AKT serine/threonine kinase 1 Homo sapiens 104-107 24685625-10 2014 HSP-70 siRNA abolished celastrol mediated cytoprotection. celastrol 23-32 heat shock protein family A (Hsp70) member 4 Homo sapiens 0-6 24685625-11 2014 CONCLUSION: This study demonstrates that celastrol reduced both LPS-induced cell death and Abeta production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NFkappaB, COX-2, and GSK-3beta expression and oxidative stress. celastrol 41-50 heat shock protein family A (Hsp70) member 4 Homo sapiens 136-142 24685625-11 2014 CONCLUSION: This study demonstrates that celastrol reduced both LPS-induced cell death and Abeta production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NFkappaB, COX-2, and GSK-3beta expression and oxidative stress. celastrol 41-50 BCL2 apoptosis regulator Homo sapiens 147-152 24685625-11 2014 CONCLUSION: This study demonstrates that celastrol reduced both LPS-induced cell death and Abeta production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NFkappaB, COX-2, and GSK-3beta expression and oxidative stress. celastrol 41-50 nuclear factor kappa B subunit 1 Homo sapiens 177-185 24685625-11 2014 CONCLUSION: This study demonstrates that celastrol reduced both LPS-induced cell death and Abeta production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NFkappaB, COX-2, and GSK-3beta expression and oxidative stress. celastrol 41-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 187-192 24685625-11 2014 CONCLUSION: This study demonstrates that celastrol reduced both LPS-induced cell death and Abeta production in vitro through increasing HSP-70 and Bcl-2 expression and reducing NFkappaB, COX-2, and GSK-3beta expression and oxidative stress. celastrol 41-50 glycogen synthase kinase 3 beta Homo sapiens 198-207 24144799-0 2014 Inhibitory effects of celastrol on rat liver cytochrome P450 1A2, 2C11, 2D6, 2E1 and 3A2 activity. celastrol 22-31 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 45-64 24144799-4 2014 Inhibition of rat CYP isoforms (IC50) by celastrol in potency order was CYP2C11 (10.2 muM)>CYP3A2 (23.2 muM)>CYP1A2 (52.8 muM)>CYP2E1 (74.2 muM)>CYP2D6 (76.4 muM). celastrol 41-50 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 72-79 24144799-4 2014 Inhibition of rat CYP isoforms (IC50) by celastrol in potency order was CYP2C11 (10.2 muM)>CYP3A2 (23.2 muM)>CYP1A2 (52.8 muM)>CYP2E1 (74.2 muM)>CYP2D6 (76.4 muM). celastrol 41-50 cytochrome P450, family 3, subfamily a, polypeptide 2 Rattus norvegicus 94-100 24144799-4 2014 Inhibition of rat CYP isoforms (IC50) by celastrol in potency order was CYP2C11 (10.2 muM)>CYP3A2 (23.2 muM)>CYP1A2 (52.8 muM)>CYP2E1 (74.2 muM)>CYP2D6 (76.4 muM). celastrol 41-50 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 115-121 24144799-4 2014 Inhibition of rat CYP isoforms (IC50) by celastrol in potency order was CYP2C11 (10.2 muM)>CYP3A2 (23.2 muM)>CYP1A2 (52.8 muM)>CYP2E1 (74.2 muM)>CYP2D6 (76.4 muM). celastrol 41-50 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 136-142 24144799-4 2014 Inhibition of rat CYP isoforms (IC50) by celastrol in potency order was CYP2C11 (10.2 muM)>CYP3A2 (23.2 muM)>CYP1A2 (52.8 muM)>CYP2E1 (74.2 muM)>CYP2D6 (76.4 muM). celastrol 41-50 cytochrome P450, family 2, subfamily d, polypeptide 4 Rattus norvegicus 157-163 24144799-5 2014 Enzyme kinetic studies showed that the celastrol was not only a competitive inhibitor of CYP1A2 and 2C11, but also a mixed-type inhibitor of CYP3A2, with Ki of 39.2 muM, 7.05 muM and 14.2 muM, respectively. celastrol 39-48 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 89-95 24144799-5 2014 Enzyme kinetic studies showed that the celastrol was not only a competitive inhibitor of CYP1A2 and 2C11, but also a mixed-type inhibitor of CYP3A2, with Ki of 39.2 muM, 7.05 muM and 14.2 muM, respectively. celastrol 39-48 cytochrome P450, family 3, subfamily a, polypeptide 2 Rattus norvegicus 141-147 24144799-6 2014 The data indicate that celastrol inhibited the metabolism of CYP1A2, 2C and 3A substrates in rat liver in vitro with a different mode of inhibition. celastrol 23-32 cytochrome P450, family 1, subfamily a, polypeptide 2 Rattus norvegicus 61-67 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 heat shock protein family A (Hsp70) member 4 Homo sapiens 89-95 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 BCL2 apoptosis regulator Homo sapiens 100-105 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 nuclear factor kappa B subunit 1 Homo sapiens 131-139 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 glycogen synthase kinase 3 beta Homo sapiens 165-195 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 glycogen synthase kinase 3 beta Homo sapiens 197-206 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 228-244 24685625-9 2014 Western blot and immunofluorescence analysis showed that exposure to celastrol increased HSP-70 and Bcl-2 expression but decreased NFkappaB activity, phosphorylated glycogen synthase kinase-3beta (GSK-3beta) at tyrosine 216 and cyclooxygenase-2 (COX-2) expression, Abeta accumulation together with a reduction of superoxide and hydrogen peroxide generation. celastrol 69-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 246-251 24111524-0 2014 Celastrol prevents cadmium-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 69-72 24111524-0 2014 Celastrol prevents cadmium-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 0-9 phosphatase and tensin homolog Homo sapiens 77-81 24111524-0 2014 Celastrol prevents cadmium-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 82-85 24111524-0 2014 Celastrol prevents cadmium-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 86-90 24111524-5 2014 This is supported by the findings that celastrol strikingly attenuated Cd-induced viability reduction, morphological change, nuclear fragmentation, and condensation, as well as activation of caspase-3 in neuronal cells. celastrol 39-48 caspase 3 Homo sapiens 191-200 24111524-6 2014 Concurrently, celastrol remarkably blocked Cd-induced phosphorylation of c-Jun N-terminal kinase (JNK), but not extracellular signal-regulated kinases 1/2 and p38, in neuronal cells. celastrol 14-23 mitogen-activated protein kinase 8 Homo sapiens 73-96 24111524-6 2014 Concurrently, celastrol remarkably blocked Cd-induced phosphorylation of c-Jun N-terminal kinase (JNK), but not extracellular signal-regulated kinases 1/2 and p38, in neuronal cells. celastrol 14-23 mitogen-activated protein kinase 8 Homo sapiens 98-101 24111524-7 2014 Inhibition of JNK by SP600125 or over-expression of dominant negative c-Jun potentiated celastrol protection against Cd-induced cell death. celastrol 88-97 mitogen-activated protein kinase 8 Homo sapiens 14-17 24111524-10 2014 The findings indicate that celastrol prevents Cd-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 27-36 mechanistic target of rapamycin kinase Homo sapiens 108-112 24111524-7 2014 Inhibition of JNK by SP600125 or over-expression of dominant negative c-Jun potentiated celastrol protection against Cd-induced cell death. celastrol 88-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-75 24111524-8 2014 Furthermore, pre-treatment with celastrol prevented Cd down-regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and activation of phosphoinositide 3"-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling in neuronal cells. celastrol 32-41 phosphatase and tensin homolog Homo sapiens 131-135 24111524-14 2014 This study underscores that celastrol prevents Cd-induced neuronal apoptosis via inhibiting activation of JNK (c-Jun N-terminal kinase) and Akt/mTOR network. celastrol 28-37 mitogen-activated protein kinase 8 Homo sapiens 106-109 24111524-8 2014 Furthermore, pre-treatment with celastrol prevented Cd down-regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and activation of phosphoinositide 3"-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling in neuronal cells. celastrol 32-41 protein tyrosine kinase 2 beta Homo sapiens 182-198 24111524-8 2014 Furthermore, pre-treatment with celastrol prevented Cd down-regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and activation of phosphoinositide 3"-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling in neuronal cells. celastrol 32-41 AKT serine/threonine kinase 1 Homo sapiens 200-203 24111524-14 2014 This study underscores that celastrol prevents Cd-induced neuronal apoptosis via inhibiting activation of JNK (c-Jun N-terminal kinase) and Akt/mTOR network. celastrol 28-37 mitogen-activated protein kinase 8 Homo sapiens 111-134 24111524-8 2014 Furthermore, pre-treatment with celastrol prevented Cd down-regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and activation of phosphoinositide 3"-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling in neuronal cells. celastrol 32-41 mechanistic target of rapamycin kinase Homo sapiens 205-234 24111524-8 2014 Furthermore, pre-treatment with celastrol prevented Cd down-regulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and activation of phosphoinositide 3"-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling in neuronal cells. celastrol 32-41 mechanistic target of rapamycin kinase Homo sapiens 236-240 24111524-9 2014 Over-expression of wild-type PTEN enhanced celastrol inhibition of Cd-activated Akt/mTOR signaling and cell death in neuronal cells. celastrol 43-52 phosphatase and tensin homolog Homo sapiens 29-33 24111524-14 2014 This study underscores that celastrol prevents Cd-induced neuronal apoptosis via inhibiting activation of JNK (c-Jun N-terminal kinase) and Akt/mTOR network. celastrol 28-37 AKT serine/threonine kinase 1 Homo sapiens 140-143 24111524-14 2014 This study underscores that celastrol prevents Cd-induced neuronal apoptosis via inhibiting activation of JNK (c-Jun N-terminal kinase) and Akt/mTOR network. celastrol 28-37 mechanistic target of rapamycin kinase Homo sapiens 144-148 24111524-15 2014 Celastrol suppresses Cd-activated Akt/mTOR pathway by elevating PTEN (phosphatase and tensin homolog). celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 34-37 24111524-9 2014 Over-expression of wild-type PTEN enhanced celastrol inhibition of Cd-activated Akt/mTOR signaling and cell death in neuronal cells. celastrol 43-52 AKT serine/threonine kinase 1 Homo sapiens 80-83 24111524-15 2014 Celastrol suppresses Cd-activated Akt/mTOR pathway by elevating PTEN (phosphatase and tensin homolog). celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 38-42 24111524-9 2014 Over-expression of wild-type PTEN enhanced celastrol inhibition of Cd-activated Akt/mTOR signaling and cell death in neuronal cells. celastrol 43-52 mechanistic target of rapamycin kinase Homo sapiens 84-88 24111524-15 2014 Celastrol suppresses Cd-activated Akt/mTOR pathway by elevating PTEN (phosphatase and tensin homolog). celastrol 0-9 phosphatase and tensin homolog Homo sapiens 64-68 24111524-10 2014 The findings indicate that celastrol prevents Cd-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 27-36 mitogen-activated protein kinase 8 Homo sapiens 91-94 24111524-10 2014 The findings indicate that celastrol prevents Cd-induced neuronal cell death via targeting JNK and PTEN-Akt/mTOR network. celastrol 27-36 phosphatase and tensin homolog Homo sapiens 99-103 24713615-7 2014 An exception was the marked response to celastrol which reduced the steady-state levels of cytoplasmic HSP90 transcripts and protein. celastrol 40-49 heat shock protein 90 alpha family class A member 1 Homo sapiens 103-108 23981709-7 2014 RESULTS: Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-alpha, interleukin-1beta, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. celastrol 9-18 tumor necrosis factor Rattus norvegicus 179-206 23981709-7 2014 RESULTS: Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-alpha, interleukin-1beta, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. celastrol 9-18 interleukin 1 beta Rattus norvegicus 208-225 23981709-7 2014 RESULTS: Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-alpha, interleukin-1beta, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. celastrol 9-18 C-C motif chemokine ligand 2 Rattus norvegicus 231-261 23981709-7 2014 RESULTS: Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-alpha, interleukin-1beta, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. celastrol 9-18 C-C motif chemokine ligand 2 Rattus norvegicus 263-268 23981709-8 2014 Moreover, celastrol prevented IR-induced expression of pro-inflammatory mediators, which was associated with suppression of nuclear translocation of NF-kappaB subunit p65. celastrol 10-19 synaptotagmin 1 Rattus norvegicus 167-170 24214023-6 2014 Similarly, celastrol treatment inhibited cytochrome c release, Bax/Bcl-2 ratio changes, and caspase-9/3 activation. celastrol 11-20 cytochrome c, somatic Homo sapiens 41-53 24214023-6 2014 Similarly, celastrol treatment inhibited cytochrome c release, Bax/Bcl-2 ratio changes, and caspase-9/3 activation. celastrol 11-20 BCL2 associated X, apoptosis regulator Homo sapiens 63-66 24214023-6 2014 Similarly, celastrol treatment inhibited cytochrome c release, Bax/Bcl-2 ratio changes, and caspase-9/3 activation. celastrol 11-20 BCL2 apoptosis regulator Homo sapiens 67-72 24214023-6 2014 Similarly, celastrol treatment inhibited cytochrome c release, Bax/Bcl-2 ratio changes, and caspase-9/3 activation. celastrol 11-20 caspase 9 Homo sapiens 92-103 24214023-7 2014 Celastrol specifically inhibited rotenone-evoked p38 mitogen-activated protein kinase activation in SH-SY5Y cells. celastrol 0-9 mitogen-activated protein kinase 14 Homo sapiens 49-85 24713615-8 2014 As Hsp90 participates in the targeting of misfolded proteins to the proteasome pathway, its down-modulation in response to celastrol may partly account for the mechanism of improved homeostasis of L444P GCase mediated by this triterpene. celastrol 123-132 heat shock protein 90 alpha family class A member 1 Homo sapiens 3-8 24144813-0 2013 Anti-invasive effects of celastrol in hypoxia-induced fibroblast-like synoviocyte through suppressing of HIF-1alpha/CXCR4 signaling pathway. celastrol 25-34 hypoxia inducible factor 1 subunit alpha Homo sapiens 105-115 24434352-0 2014 Celastrol induces apoptosis of gastric cancer cells by miR-21 inhibiting PI3K/Akt-NF-kappaB signaling pathway. celastrol 0-9 microRNA 21 Homo sapiens 55-61 24434352-0 2014 Celastrol induces apoptosis of gastric cancer cells by miR-21 inhibiting PI3K/Akt-NF-kappaB signaling pathway. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 78-81 24434352-0 2014 Celastrol induces apoptosis of gastric cancer cells by miR-21 inhibiting PI3K/Akt-NF-kappaB signaling pathway. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 82-91 24434352-3 2014 METHODS: The effect of celastrol on PI3K/Akt and the NF-kappaB signaling pathway was evaluated with Western blot and luciferase reporter assay. celastrol 23-32 AKT serine/threonine kinase 1 Homo sapiens 41-44 24434352-3 2014 METHODS: The effect of celastrol on PI3K/Akt and the NF-kappaB signaling pathway was evaluated with Western blot and luciferase reporter assay. celastrol 23-32 nuclear factor kappa B subunit 1 Homo sapiens 53-62 24434352-6 2014 RESULTS: It was identified that celastrol was capable of inducing apoptosis of gastric cancer cells, which was mediated via inhibiting the activation of PI3K/Akt and NF-kappaB. celastrol 32-41 AKT serine/threonine kinase 1 Homo sapiens 158-161 24434352-6 2014 RESULTS: It was identified that celastrol was capable of inducing apoptosis of gastric cancer cells, which was mediated via inhibiting the activation of PI3K/Akt and NF-kappaB. celastrol 32-41 nuclear factor kappa B subunit 1 Homo sapiens 166-175 24434352-7 2014 A strong activator of Akt, IGF-1 restored NF-kappaB activity in cells treated with celastrol. celastrol 83-92 AKT serine/threonine kinase 1 Homo sapiens 22-25 24434352-7 2014 A strong activator of Akt, IGF-1 restored NF-kappaB activity in cells treated with celastrol. celastrol 83-92 insulin like growth factor 1 Homo sapiens 27-32 24434352-7 2014 A strong activator of Akt, IGF-1 restored NF-kappaB activity in cells treated with celastrol. celastrol 83-92 nuclear factor kappa B subunit 1 Homo sapiens 42-51 24434352-8 2014 Celastrol could also significantly suppress miR-21 expression. celastrol 0-9 microRNA 21 Homo sapiens 44-50 24434352-10 2014 Notably, upregulation of miR-21 expression can increase PI3K/Akt and NF-kappaB activity and decrease apoptosis of gastric cancer cells treated with celastrol, which could be reversed by PI3K inhibitor. celastrol 148-157 microRNA 21 Homo sapiens 25-31 24434352-10 2014 Notably, upregulation of miR-21 expression can increase PI3K/Akt and NF-kappaB activity and decrease apoptosis of gastric cancer cells treated with celastrol, which could be reversed by PI3K inhibitor. celastrol 148-157 AKT serine/threonine kinase 1 Homo sapiens 61-64 24434352-10 2014 Notably, upregulation of miR-21 expression can increase PI3K/Akt and NF-kappaB activity and decrease apoptosis of gastric cancer cells treated with celastrol, which could be reversed by PI3K inhibitor. celastrol 148-157 nuclear factor kappa B subunit 1 Homo sapiens 69-78 24434352-11 2014 CONCLUSIONS: Our data revealed that the effect of celastrol on apoptosis was due to miR-21 inhibiting the PI3K/Akt-dependent NF-kappaB pathway. celastrol 50-59 microRNA 21 Homo sapiens 84-90 24434352-11 2014 CONCLUSIONS: Our data revealed that the effect of celastrol on apoptosis was due to miR-21 inhibiting the PI3K/Akt-dependent NF-kappaB pathway. celastrol 50-59 AKT serine/threonine kinase 1 Homo sapiens 111-114 24434352-11 2014 CONCLUSIONS: Our data revealed that the effect of celastrol on apoptosis was due to miR-21 inhibiting the PI3K/Akt-dependent NF-kappaB pathway. celastrol 50-59 nuclear factor kappa B subunit 1 Homo sapiens 125-134 24144813-9 2013 Meanwhile, it is revealed that celastrol inhibited the transcriptional activity of CXCR4 under hypoxic conditions by suppressing the binding activity of HIF-1alpha in the CXCR4 promoter, and blocked hypoxia-induced accumulation of nuclear HIF-1alpha. celastrol 31-40 C-X-C motif chemokine receptor 4 Homo sapiens 83-88 24144813-9 2013 Meanwhile, it is revealed that celastrol inhibited the transcriptional activity of CXCR4 under hypoxic conditions by suppressing the binding activity of HIF-1alpha in the CXCR4 promoter, and blocked hypoxia-induced accumulation of nuclear HIF-1alpha. celastrol 31-40 hypoxia inducible factor 1 subunit alpha Homo sapiens 153-163 24144813-9 2013 Meanwhile, it is revealed that celastrol inhibited the transcriptional activity of CXCR4 under hypoxic conditions by suppressing the binding activity of HIF-1alpha in the CXCR4 promoter, and blocked hypoxia-induced accumulation of nuclear HIF-1alpha. celastrol 31-40 C-X-C motif chemokine receptor 4 Homo sapiens 171-176 24144813-9 2013 Meanwhile, it is revealed that celastrol inhibited the transcriptional activity of CXCR4 under hypoxic conditions by suppressing the binding activity of HIF-1alpha in the CXCR4 promoter, and blocked hypoxia-induced accumulation of nuclear HIF-1alpha. celastrol 31-40 hypoxia inducible factor 1 subunit alpha Homo sapiens 239-249 24144813-11 2013 In conclusion, our results indicate that celastrol inhibits hypoxia-induced migration and invasion via suppression of HIF-1alpha mediated CXCR4 expression in FLSs under hypoxic conditions. celastrol 41-50 hypoxia inducible factor 1 subunit alpha Homo sapiens 118-128 24144813-11 2013 In conclusion, our results indicate that celastrol inhibits hypoxia-induced migration and invasion via suppression of HIF-1alpha mediated CXCR4 expression in FLSs under hypoxic conditions. celastrol 41-50 C-X-C motif chemokine receptor 4 Homo sapiens 138-143 24144813-0 2013 Anti-invasive effects of celastrol in hypoxia-induced fibroblast-like synoviocyte through suppressing of HIF-1alpha/CXCR4 signaling pathway. celastrol 25-34 C-X-C motif chemokine receptor 4 Homo sapiens 116-121 24144813-8 2013 In addition, we also found that celastrol inhibited hypoxia-induced CXCR4 expression at both the mRNA and the protein levels in RA-FLSs. celastrol 32-41 C-X-C motif chemokine receptor 4 Homo sapiens 68-73 24056254-10 2013 Very interestingly, Sulforaphane, Withaferin A, Celastrol and EGCG all decreased the complemented NRL-Hsp90alpha/Cdc37-CRL activities in the concentration-dependent manner. celastrol 48-57 heat shock protein 90 alpha family class A member 1 Homo sapiens 102-112 24056254-10 2013 Very interestingly, Sulforaphane, Withaferin A, Celastrol and EGCG all decreased the complemented NRL-Hsp90alpha/Cdc37-CRL activities in the concentration-dependent manner. celastrol 48-57 cell division cycle 37, HSP90 cochaperone Homo sapiens 113-118 24056254-10 2013 Very interestingly, Sulforaphane, Withaferin A, Celastrol and EGCG all decreased the complemented NRL-Hsp90alpha/Cdc37-CRL activities in the concentration-dependent manner. celastrol 48-57 interleukin 31 receptor A Homo sapiens 119-122 23734772-8 2013 CONCLUSION: These results suggest that 4E-BP1 plays a critical role in the mechanism by which TRAIL and celastrol together cause apoptotic cell death in human pancreatic tumour cells. celastrol 104-113 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 39-45 23583203-6 2013 The results showed that silencing of Hsp70 by chitosan-TPP-Hsp70 siRNA treatment significantly reduced cell viability, and enhanced antiproliferative effects of celastrol in leukemia and glioblastoma cells. celastrol 161-170 heat shock protein family A (Hsp70) member 4 Homo sapiens 37-42 23583203-6 2013 The results showed that silencing of Hsp70 by chitosan-TPP-Hsp70 siRNA treatment significantly reduced cell viability, and enhanced antiproliferative effects of celastrol in leukemia and glioblastoma cells. celastrol 161-170 heat shock protein family A (Hsp70) member 4 Homo sapiens 59-64 23734772-0 2013 Role of the eIF4E binding protein 4E-BP1 in regulation of the sensitivity of human pancreatic cancer cells to TRAIL and celastrol-induced apoptosis. celastrol 120-129 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 34-40 23850675-0 2013 Celastrol inhibits TGF-beta1-induced epithelial-mesenchymal transition by inhibiting Snail and regulating E-cadherin expression. celastrol 0-9 transforming growth factor beta-1 proprotein Canis lupus familiaris 19-28 23734772-2 2013 Although human pancreatic cancer cells show varying degrees of response they can be sensitised to the pro-apoptotic effects of TRAIL in the presence of celastrol, a natural compound extracted from the plant Tripterygium wilfordii Hook F. One important aspect of the cellular response to TRAIL is the control of protein synthesis, a key regulator of which is the eukaryotic initiation factor 4E-binding protein, 4E-BP1. celastrol 152-161 TNF superfamily member 10 Homo sapiens 127-132 23734772-2 2013 Although human pancreatic cancer cells show varying degrees of response they can be sensitised to the pro-apoptotic effects of TRAIL in the presence of celastrol, a natural compound extracted from the plant Tripterygium wilfordii Hook F. One important aspect of the cellular response to TRAIL is the control of protein synthesis, a key regulator of which is the eukaryotic initiation factor 4E-binding protein, 4E-BP1. celastrol 152-161 TNF superfamily member 10 Homo sapiens 287-292 23734772-2 2013 Although human pancreatic cancer cells show varying degrees of response they can be sensitised to the pro-apoptotic effects of TRAIL in the presence of celastrol, a natural compound extracted from the plant Tripterygium wilfordii Hook F. One important aspect of the cellular response to TRAIL is the control of protein synthesis, a key regulator of which is the eukaryotic initiation factor 4E-binding protein, 4E-BP1. celastrol 152-161 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 411-417 23734772-4 2013 In cells that are normally resistant to TRAIL, synergistic effects of TRAIL plus celastrol on commitment to apoptosis and inhibition of protein synthesis were observed. celastrol 81-90 TNF superfamily member 10 Homo sapiens 40-45 23239560-0 2013 AFM studied the effect of celastrol on beta1 integrin-mediated HUVEC adhesion and migration. celastrol 26-35 integrin subunit beta 1 Homo sapiens 39-53 23239560-3 2013 Here, the mechanism underling the antiangiogenesis capacity of celastrol was investigated by exploring the effect of celastrol on beta1(CD29) integrin-mediated cell adhesion and migration. celastrol 63-72 integrin subunit beta 1 Homo sapiens 136-140 23239560-3 2013 Here, the mechanism underling the antiangiogenesis capacity of celastrol was investigated by exploring the effect of celastrol on beta1(CD29) integrin-mediated cell adhesion and migration. celastrol 117-126 integrin subunit beta 1 Homo sapiens 136-140 23239560-4 2013 Flow cytometry results showed that the HUVECs highly expressed CD29 and cell adhesion assay indicated that celastrol specifically inhibited the adhesion of HUVECs to fibronectin (FN) without affecting nonspecific adhesion to poly-L-lysine (PLL). celastrol 107-116 integrin subunit beta 1 Homo sapiens 63-67 23239560-4 2013 Flow cytometry results showed that the HUVECs highly expressed CD29 and cell adhesion assay indicated that celastrol specifically inhibited the adhesion of HUVECs to fibronectin (FN) without affecting nonspecific adhesion to poly-L-lysine (PLL). celastrol 107-116 fibronectin 1 Homo sapiens 166-177 23239560-4 2013 Flow cytometry results showed that the HUVECs highly expressed CD29 and cell adhesion assay indicated that celastrol specifically inhibited the adhesion of HUVECs to fibronectin (FN) without affecting nonspecific adhesion to poly-L-lysine (PLL). celastrol 107-116 fibronectin 1 Homo sapiens 179-181 23239560-10 2013 Taken together, our results suggest that celastrol can be as an inhibitor of HUVEC adhesion to FN. celastrol 41-50 fibronectin 1 Homo sapiens 95-97 23810294-0 2013 Inhibition of C2C12 myotube atrophy by a novel HSP70 inducer, celastrol, via activation of Akt1 and ERK1/2 pathways. celastrol 62-71 heat shock protein family A (Hsp70) member 4 Homo sapiens 47-52 23810294-0 2013 Inhibition of C2C12 myotube atrophy by a novel HSP70 inducer, celastrol, via activation of Akt1 and ERK1/2 pathways. celastrol 62-71 AKT serine/threonine kinase 1 Homo sapiens 91-95 23810294-0 2013 Inhibition of C2C12 myotube atrophy by a novel HSP70 inducer, celastrol, via activation of Akt1 and ERK1/2 pathways. celastrol 62-71 mitogen-activated protein kinase 3 Homo sapiens 100-106 23810294-1 2013 Celastrol (CEL) is known as a potent inducer of heat shock protein (HSP) in non-muscle cells and exhibits cytoprotective function and inhibitory effects on proteasome and glucocorticoid receptor activities. celastrol 0-9 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 48-66 23810294-1 2013 Celastrol (CEL) is known as a potent inducer of heat shock protein (HSP) in non-muscle cells and exhibits cytoprotective function and inhibitory effects on proteasome and glucocorticoid receptor activities. celastrol 0-9 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 68-71 23810294-1 2013 Celastrol (CEL) is known as a potent inducer of heat shock protein (HSP) in non-muscle cells and exhibits cytoprotective function and inhibitory effects on proteasome and glucocorticoid receptor activities. celastrol 11-14 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 48-66 23810294-1 2013 Celastrol (CEL) is known as a potent inducer of heat shock protein (HSP) in non-muscle cells and exhibits cytoprotective function and inhibitory effects on proteasome and glucocorticoid receptor activities. celastrol 11-14 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 68-71 23810294-6 2013 Inhibition of Akt1 and ERK1/2 pathways by specific inhibitors confirmed CEL-induced anti-atrophic effect. celastrol 72-75 AKT serine/threonine kinase 1 Homo sapiens 14-18 23810294-6 2013 Inhibition of Akt1 and ERK1/2 pathways by specific inhibitors confirmed CEL-induced anti-atrophic effect. celastrol 72-75 mitogen-activated protein kinase 3 Homo sapiens 23-29 23850675-0 2013 Celastrol inhibits TGF-beta1-induced epithelial-mesenchymal transition by inhibiting Snail and regulating E-cadherin expression. celastrol 0-9 cadherin 1 Canis lupus familiaris 106-116 23850675-5 2013 The downregulation of E-cadherin expression and upregulation of Snail in Madin-Darby Canine Kidney (MDCK) and A549 cell lines show that TGF-beta1-mediated the EMT in epithelial cells; however, celastrol markedly inhibited TGF-beta1-induced morphologic changes, Snail upregulation, and E-cadherin expression. celastrol 193-202 transforming growth factor beta-1 proprotein Canis lupus familiaris 136-145 23850675-6 2013 Migration and invasion assays revealed that celastrol completely inhibited TGF-beta1-mediated cellular migration in both cell lines. celastrol 44-53 transforming growth factor beta-1 proprotein Canis lupus familiaris 75-84 23850675-7 2013 These findings indicate that celastrol downregulates Snail expression, thereby inhibiting TGF-beta1-induced EMT in MDCK and A549 cells. celastrol 29-38 transforming growth factor beta-1 proprotein Canis lupus familiaris 90-99 23850675-8 2013 Thus, our findings provide new evidence that celastrol suppresses lung cancer invasion and migration by inhibiting TGF-beta1-induced EMT. celastrol 45-54 transforming growth factor beta-1 proprotein Canis lupus familiaris 115-124 23861949-6 2013 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppressing the binding activity of NF-kappaB in the MMP-9 promoter, and suppressed the TLR4/MyD88/NF-kappaB pathway. celastrol 39-48 matrix metallopeptidase 9 Homo sapiens 91-96 23846217-3 2013 Proteasome catalytic subunit beta1 was predicted by computational analysis to be a possible direct target of celastrol and confirmed by checking direct effect of celastrol on the activity of recombinant human proteasome subunit beta1 in vitro. celastrol 109-118 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 29-34 23846217-3 2013 Proteasome catalytic subunit beta1 was predicted by computational analysis to be a possible direct target of celastrol and confirmed by checking direct effect of celastrol on the activity of recombinant human proteasome subunit beta1 in vitro. celastrol 109-118 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 228-233 23846217-3 2013 Proteasome catalytic subunit beta1 was predicted by computational analysis to be a possible direct target of celastrol and confirmed by checking direct effect of celastrol on the activity of recombinant human proteasome subunit beta1 in vitro. celastrol 162-171 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 29-34 23846217-3 2013 Proteasome catalytic subunit beta1 was predicted by computational analysis to be a possible direct target of celastrol and confirmed by checking direct effect of celastrol on the activity of recombinant human proteasome subunit beta1 in vitro. celastrol 162-171 UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2 Homo sapiens 228-233 23846217-5 2013 Possible target-related proteins of celastrol such as endoplasmic reticulum protein 29 (ERP29) and mitochondrial import receptor Tom22 (TOM22) were found by 2-DE analysis of total cellular protein expression profiles. celastrol 36-45 endoplasmic reticulum protein 29 Homo sapiens 54-86 23846217-5 2013 Possible target-related proteins of celastrol such as endoplasmic reticulum protein 29 (ERP29) and mitochondrial import receptor Tom22 (TOM22) were found by 2-DE analysis of total cellular protein expression profiles. celastrol 36-45 endoplasmic reticulum protein 29 Homo sapiens 88-93 23846217-5 2013 Possible target-related proteins of celastrol such as endoplasmic reticulum protein 29 (ERP29) and mitochondrial import receptor Tom22 (TOM22) were found by 2-DE analysis of total cellular protein expression profiles. celastrol 36-45 translocase of outer mitochondrial membrane 22 Homo sapiens 99-134 23846217-5 2013 Possible target-related proteins of celastrol such as endoplasmic reticulum protein 29 (ERP29) and mitochondrial import receptor Tom22 (TOM22) were found by 2-DE analysis of total cellular protein expression profiles. celastrol 36-45 translocase of outer mitochondrial membrane 22 Homo sapiens 136-141 23846217-7 2013 Celastrol induced translocation of Bax into the mitochondria, which might be related to the upregulation of BH-3-only proteins such as BIM and the increase in the expression level of TOM22. celastrol 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 35-38 23846217-7 2013 Celastrol induced translocation of Bax into the mitochondria, which might be related to the upregulation of BH-3-only proteins such as BIM and the increase in the expression level of TOM22. celastrol 0-9 translocase of outer mitochondrial membrane 22 Homo sapiens 183-188 23846217-10 2013 The important role of glycogen synthase kinase-3beta (GSK3beta) in the signal cascades of celastrol was suggested. celastrol 90-99 glycogen synthase kinase 3 beta Homo sapiens 22-52 23846217-10 2013 The important role of glycogen synthase kinase-3beta (GSK3beta) in the signal cascades of celastrol was suggested. celastrol 90-99 glycogen synthase kinase 3 beta Homo sapiens 54-62 23846217-11 2013 Pretreatment of LiCL, an inhibitor of GSK3beta, could significantly ameliorate apoptosis induced by celastrol. celastrol 100-109 glycogen synthase kinase 3 beta Homo sapiens 38-46 23861949-0 2013 Celastrol inhibits lipopolysaccharide-stimulated rheumatoid fibroblast-like synoviocyte invasion through suppression of TLR4/NF-kappaB-mediated matrix metalloproteinase-9 expression. celastrol 0-9 toll like receptor 4 Homo sapiens 120-124 23861949-5 2013 Results showed that celastrol suppressed LPS-stimulated FLS migration and invasion by inhibiting MMP-9 expression and activity. celastrol 20-29 matrix metallopeptidase 9 Homo sapiens 97-102 23861949-6 2013 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppressing the binding activity of NF-kappaB in the MMP-9 promoter, and suppressed the TLR4/MyD88/NF-kappaB pathway. celastrol 39-48 matrix metallopeptidase 9 Homo sapiens 153-158 23861949-6 2013 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppressing the binding activity of NF-kappaB in the MMP-9 promoter, and suppressed the TLR4/MyD88/NF-kappaB pathway. celastrol 39-48 toll like receptor 4 Homo sapiens 188-192 23861949-6 2013 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppressing the binding activity of NF-kappaB in the MMP-9 promoter, and suppressed the TLR4/MyD88/NF-kappaB pathway. celastrol 39-48 MYD88 innate immune signal transduction adaptor Homo sapiens 193-198 23861949-8 2013 In conclusion, celastrol might inhibit FLS migration and invasion induced by LPS by suppressing TLR4/NF-kappaB-mediated MMP-9 expression, providing a theoretical foundation for the clinical treatment of RA with celastrol. celastrol 15-24 toll like receptor 4 Homo sapiens 96-100 23861949-8 2013 In conclusion, celastrol might inhibit FLS migration and invasion induced by LPS by suppressing TLR4/NF-kappaB-mediated MMP-9 expression, providing a theoretical foundation for the clinical treatment of RA with celastrol. celastrol 15-24 matrix metallopeptidase 9 Homo sapiens 120-125 23861949-8 2013 In conclusion, celastrol might inhibit FLS migration and invasion induced by LPS by suppressing TLR4/NF-kappaB-mediated MMP-9 expression, providing a theoretical foundation for the clinical treatment of RA with celastrol. celastrol 211-220 toll like receptor 4 Homo sapiens 96-100 23861949-8 2013 In conclusion, celastrol might inhibit FLS migration and invasion induced by LPS by suppressing TLR4/NF-kappaB-mediated MMP-9 expression, providing a theoretical foundation for the clinical treatment of RA with celastrol. celastrol 211-220 matrix metallopeptidase 9 Homo sapiens 120-125 23618875-0 2013 Heterogeneity in the properties of NEFL mutants causing Charcot-Marie-Tooth disease results in differential effects on neurofilament assembly and susceptibility to intervention by the chaperone-inducer, celastrol. celastrol 203-212 neurofilament, light polypeptide Mus musculus 35-39 23618875-7 2013 Celastrol, an inducer of chaperone proteins, induced HSPA1 expression in motor neurons and prevented the formation of neurofilament inclusions and mitochondrial shortening induced by expression of NEFL(Q333P), but not in sensory neurons. celastrol 0-9 neurofilament, light polypeptide Mus musculus 197-201 23618875-8 2013 Conversely, celastrol had a protective effect against the toxicity of NEFL(P8R), a mutant which is sensitive to HSBP1 but not HSPA1 chaperoning, only in large-sized sensory neurons, not in motor neurons. celastrol 12-21 neurofilament, light polypeptide Mus musculus 70-74 23618875-8 2013 Conversely, celastrol had a protective effect against the toxicity of NEFL(P8R), a mutant which is sensitive to HSBP1 but not HSPA1 chaperoning, only in large-sized sensory neurons, not in motor neurons. celastrol 12-21 heat shock factor binding protein 1 Mus musculus 112-117 23485335-5 2013 MnSOD was up-regulated by MG132 and celastrol, and GST-pi was up-regulated by MG132 and lactacystin. celastrol 36-45 superoxide dismutase 2 Homo sapiens 0-5 23649759-0 2013 Celastrol exerts synergistic effects with PHA-665752 and inhibits tumor growth of c-Met-deficient hepatocellular carcinoma in vivo. celastrol 0-9 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 82-87 23649759-6 2013 Our results showed that Celastrol at high concentration (>1.0 muM) induced G2/M arrest and apoptosis with the activation of Caspase3/7 in Huh7 cells whereas at low concentration (<1.0 muM) had no obvious effects. celastrol 24-33 caspase 3 Homo sapiens 127-135 23799016-0 2013 Celastrol prevents atherosclerosis via inhibiting LOX-1 and oxidative stress. celastrol 0-9 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 50-55 23649759-6 2013 Our results showed that Celastrol at high concentration (>1.0 muM) induced G2/M arrest and apoptosis with the activation of Caspase3/7 in Huh7 cells whereas at low concentration (<1.0 muM) had no obvious effects. celastrol 24-33 MIR7-3 host gene Homo sapiens 141-145 23649759-7 2013 Low concentration Celastrol presented significant combined effects with PHA on Huh7 cells and Huh7 xenografts in terms of growth inhibition, migration inhibition and apoptosis induction. celastrol 18-27 MIR7-3 host gene Homo sapiens 79-83 23649759-7 2013 Low concentration Celastrol presented significant combined effects with PHA on Huh7 cells and Huh7 xenografts in terms of growth inhibition, migration inhibition and apoptosis induction. celastrol 18-27 MIR7-3 host gene Homo sapiens 94-98 23649759-8 2013 These results suggest that Celastrol and its combination with PHA present the therapeutic potential on c-Met-deficient hepatocellular carcinoma, and deserve further preclinical and clinical studies. celastrol 27-36 MET proto-oncogene, receptor tyrosine kinase Homo sapiens 103-108 23799016-4 2013 We found that celastrol significantly attenuated oxLDL-induced excessive expression of lectin-like oxidized low density lipoprotein receptor-1(LOX-1) and generation of reactive oxygen species (ROS) in cultured RAW264.7 macrophages. celastrol 14-23 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 143-148 23799016-5 2013 Celastrol also decreased IkappaB phosphorylation and degradation and reduced production of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and IL-6. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 91-122 23799016-5 2013 Celastrol also decreased IkappaB phosphorylation and degradation and reduced production of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and IL-6. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 124-128 23799016-5 2013 Celastrol also decreased IkappaB phosphorylation and degradation and reduced production of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and IL-6. celastrol 0-9 tumor necrosis factor Mus musculus 187-220 23799016-5 2013 Celastrol also decreased IkappaB phosphorylation and degradation and reduced production of inducible nitric oxide synthase (iNOS), nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and IL-6. celastrol 0-9 interleukin 6 Mus musculus 225-229 23799016-7 2013 The expression of LOX-1 within the atherosclerotic lesions and generation of superoxide in mouse aorta were also significantly reduced by celastrol while the lipid profile was not improved. celastrol 138-147 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 18-23 23497885-3 2013 Of the non-flavonoid phytochemicals tested, berberine, celastrol, ellagic acid, limonin, oleanolic acid, propyl gallate, sinapic acid and ursolic acid demonstrated significant inhibition of ABCG2-mediated transport. celastrol 55-64 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 190-195 23799016-8 2013 In conclusion, our results show that celastrol inhibits atherosclerotic plaque developing in apoE(-/-) mice via inhibiting LOX-1 and oxidative stress. celastrol 37-46 oxidized low density lipoprotein (lectin-like) receptor 1 Mus musculus 123-128 23706078-0 2013 Celastrol induces apoptosis of gastric cancer cells by miR-146a inhibition of NF-kappaB activity. celastrol 0-9 microRNA 146a Homo sapiens 55-63 23706078-5 2013 Finally, the effect of miR-146a on celastrol-induced anti-tumor activity was assessed using miR-146a inhibitor. celastrol 35-44 microRNA 146a Homo sapiens 23-31 23706078-5 2013 Finally, the effect of miR-146a on celastrol-induced anti-tumor activity was assessed using miR-146a inhibitor. celastrol 35-44 microRNA 146a Homo sapiens 92-100 23706078-7 2013 Celastrol also reduced IkappaB phosphorylation, nuclear P65 protein levels and NF-kappaB activity. celastrol 0-9 RELA proto-oncogene, NF-kB subunit Homo sapiens 56-59 23706078-8 2013 Furthermore, Celastrol could increase miR-146a expression and up-regulation of miR-146a expression could suppress NF-kappaB activity. celastrol 13-22 microRNA 146a Homo sapiens 38-46 23706078-9 2013 More important, down-regulation of miR-146a expression can reverse the effect of celastrol on NF-kappaB activity and apoptosis in gastric cancer cells. celastrol 81-90 microRNA 146a Homo sapiens 35-43 23706078-10 2013 CONCLUSIONS: In this study, we demonstrated that the effect of celastrol on apoptosis is due to miR-146a inhibition of NF-kappaB activity. celastrol 63-72 microRNA 146a Homo sapiens 96-104 23142250-5 2013 RESULTS: Anti-proliferation and apoptotic effects of celastrol were demonstrated by CCK-8 assay, Annexin-V/PI staining method, mitochondrial membrane potential (deltapsim) assay and caspase-3 assay. celastrol 53-62 annexin A5 Homo sapiens 97-106 23637966-0 2013 Celastrol, an NF-kappaB inhibitor, improves insulin resistance and attenuates renal injury in db/db mice. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 14-23 23637966-4 2013 We investigated the effects of the NF-kappaB inhibitor celastrol in db/db mice. celastrol 55-64 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 35-44 23637966-7 2013 Celastrol reduced insulin resistance and lipid abnormalities and led to higher plasma adiponectin levels. celastrol 0-9 adiponectin, C1Q and collagen domain containing Mus musculus 86-97 23637966-10 2013 Celastrol treatment significantly lowered mesangial expansion and suppressed type IV collagen, PAI-1 and TGFbeta1 expressions in renal tissues. celastrol 0-9 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 95-100 23637966-10 2013 Celastrol treatment significantly lowered mesangial expansion and suppressed type IV collagen, PAI-1 and TGFbeta1 expressions in renal tissues. celastrol 0-9 transforming growth factor, beta 1 Mus musculus 105-113 23266469-6 2013 Inhibition of AMPK blocked celastrol-mediated p53 phosphorylation. celastrol 27-36 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 14-18 23266469-6 2013 Inhibition of AMPK blocked celastrol-mediated p53 phosphorylation. celastrol 27-36 tumor protein p53 Homo sapiens 46-49 23266469-7 2013 Moreover, celastrol increased the expression of tumor suppressor polo like kinase-2 (PLK-2) in a p53-dependent manner. celastrol 10-19 polo like kinase 2 Homo sapiens 85-90 23266469-7 2013 Moreover, celastrol increased the expression of tumor suppressor polo like kinase-2 (PLK-2) in a p53-dependent manner. celastrol 10-19 tumor protein p53 Homo sapiens 97-100 23266469-9 2013 Furthermore, add-back of PLK-2 resulted in an increase in both celastrol-mediated PARP-2 induction and celastrol-induced apoptotic index sub G1 population. celastrol 63-72 polo like kinase 2 Homo sapiens 25-30 23266469-9 2013 Furthermore, add-back of PLK-2 resulted in an increase in both celastrol-mediated PARP-2 induction and celastrol-induced apoptotic index sub G1 population. celastrol 63-72 poly(ADP-ribose) polymerase 2 Homo sapiens 82-88 23266469-9 2013 Furthermore, add-back of PLK-2 resulted in an increase in both celastrol-mediated PARP-2 induction and celastrol-induced apoptotic index sub G1 population. celastrol 103-112 polo like kinase 2 Homo sapiens 25-30 23266469-10 2013 Together, these results suggest that celastrol may have anti-tumor effects on MCF-7 cells via AMPK-induced p53 and PLK-2 pathways. celastrol 37-46 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 94-98 23266469-10 2013 Together, these results suggest that celastrol may have anti-tumor effects on MCF-7 cells via AMPK-induced p53 and PLK-2 pathways. celastrol 37-46 tumor protein p53 Homo sapiens 107-110 23266469-10 2013 Together, these results suggest that celastrol may have anti-tumor effects on MCF-7 cells via AMPK-induced p53 and PLK-2 pathways. celastrol 37-46 polo like kinase 2 Homo sapiens 115-120 23396231-0 2013 Celastrol, an inhibitor of heat shock protein 90beta potently suppresses the expression of matrix metalloproteinases, inducible nitric oxide synthase and cyclooxygenase-2 in primary human osteoarthritic chondrocytes. celastrol 0-9 nitric oxide synthase 2 Homo sapiens 118-149 23396231-0 2013 Celastrol, an inhibitor of heat shock protein 90beta potently suppresses the expression of matrix metalloproteinases, inducible nitric oxide synthase and cyclooxygenase-2 in primary human osteoarthritic chondrocytes. celastrol 0-9 prostaglandin-endoperoxide synthase 2 Homo sapiens 154-170 23396231-6 2013 We found that treatment of primary human osteoarthritic chondrocytes with various concentrations of celastrol resulted in striking decrease in the expression of MMP-1, MMP-3, MMP-13, iNOS-2 and COX-2. celastrol 100-109 matrix metallopeptidase 1 Homo sapiens 161-166 23396231-6 2013 We found that treatment of primary human osteoarthritic chondrocytes with various concentrations of celastrol resulted in striking decrease in the expression of MMP-1, MMP-3, MMP-13, iNOS-2 and COX-2. celastrol 100-109 matrix metallopeptidase 3 Homo sapiens 168-173 23396231-6 2013 We found that treatment of primary human osteoarthritic chondrocytes with various concentrations of celastrol resulted in striking decrease in the expression of MMP-1, MMP-3, MMP-13, iNOS-2 and COX-2. celastrol 100-109 matrix metallopeptidase 13 Homo sapiens 175-181 23396231-6 2013 We found that treatment of primary human osteoarthritic chondrocytes with various concentrations of celastrol resulted in striking decrease in the expression of MMP-1, MMP-3, MMP-13, iNOS-2 and COX-2. celastrol 100-109 nitric oxide synthase 2 Homo sapiens 183-187 23396231-6 2013 We found that treatment of primary human osteoarthritic chondrocytes with various concentrations of celastrol resulted in striking decrease in the expression of MMP-1, MMP-3, MMP-13, iNOS-2 and COX-2. celastrol 100-109 prostaglandin-endoperoxide synthase 2 Homo sapiens 194-199 23396231-7 2013 In addition, celastrol treatment of cells also inhibited the activation of nuclear factor-kappa B (NF-kappaB). celastrol 13-22 nuclear factor kappa B subunit 1 Homo sapiens 75-97 23396231-7 2013 In addition, celastrol treatment of cells also inhibited the activation of nuclear factor-kappa B (NF-kappaB). celastrol 13-22 nuclear factor kappa B subunit 1 Homo sapiens 99-108 23396231-8 2013 Taken together, we provide evidence that celastrol can protect human chondrocytes by downregulating the expression of MMPs, iNOS and COX-2. celastrol 41-50 nitric oxide synthase 2 Homo sapiens 124-128 23396231-8 2013 Taken together, we provide evidence that celastrol can protect human chondrocytes by downregulating the expression of MMPs, iNOS and COX-2. celastrol 41-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 133-138 23266469-0 2013 Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 64-92 23266469-0 2013 Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 94-98 23266469-0 2013 Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway. celastrol 0-9 tumor protein p53 Homo sapiens 108-111 23266469-0 2013 Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway. celastrol 0-9 polo like kinase 2 Homo sapiens 132-137 23266469-2 2013 In this study, we found that celastrol suppressed the viability of breast cancer MCF-7 cells in an AMP-activated protein kinase (AMPK)-dependent fashion. celastrol 29-38 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 99-127 23266469-2 2013 In this study, we found that celastrol suppressed the viability of breast cancer MCF-7 cells in an AMP-activated protein kinase (AMPK)-dependent fashion. celastrol 29-38 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 129-133 23266469-3 2013 Celastrol also induced an increase in reactive oxygen species (ROS) levels, leading to AMPK phosphorylation. celastrol 0-9 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 87-91 23266469-4 2013 Protein kinase C (PKC) zeta was also shown to play a role in celastrol-induced ROS generation. celastrol 61-70 protein kinase C zeta Homo sapiens 0-27 23266469-5 2013 In addition, celastrol increased phosphorylation of the pro-apoptotic effector, p53. celastrol 13-22 tumor protein p53 Homo sapiens 80-83 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 13-17 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 transforming growth factor beta 1 Homo sapiens 112-121 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 149-153 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 RELA proto-oncogene, NF-kB subunit Homo sapiens 158-162 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 transforming growth factor beta 1 Homo sapiens 186-195 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 tumor necrosis factor Homo sapiens 201-228 22641218-9 2013 Celastrol, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-beta1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-beta1- and tumor necrosis factor-alpha (TNF-alpha)-induced NF-kappaB reporter gene activity. celastrol 0-9 tumor necrosis factor Homo sapiens 230-239 22641218-10 2013 Celastrol also inhibited cell proliferation, while increasing sub-G0 DNA fragmentation and Annexin V markers of apoptosis. celastrol 0-9 annexin A5 Homo sapiens 91-100 22641218-15 2013 Celastrol highlights the therapeutic potential of agents targeting TAK1 as a key node in this pro-oncogenic TGF-beta-NF-kappaB signal pathway. celastrol 0-9 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 67-71 22641218-15 2013 Celastrol highlights the therapeutic potential of agents targeting TAK1 as a key node in this pro-oncogenic TGF-beta-NF-kappaB signal pathway. celastrol 0-9 transforming growth factor beta 1 Homo sapiens 108-116 23142250-5 2013 RESULTS: Anti-proliferation and apoptotic effects of celastrol were demonstrated by CCK-8 assay, Annexin-V/PI staining method, mitochondrial membrane potential (deltapsim) assay and caspase-3 assay. celastrol 53-62 caspase 3 Homo sapiens 182-191 22949384-6 2013 The macrophage-conditioned media promoted SMC proliferation and MMP-2 production, which was dampened by 10-100 nM celastrol. celastrol 114-123 matrix metallopeptidase 2 Homo sapiens 64-69 22865541-8 2013 Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. celastrol 26-35 heat shock protein family A (Hsp70) member 4 Homo sapiens 186-191 22865541-8 2013 Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. celastrol 26-35 heat shock protein family B (small) member 1 Homo sapiens 193-198 22865541-8 2013 Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. celastrol 26-35 heme oxygenase 1 Homo sapiens 203-208 22949384-9 2013 The resistin-induced shedding of integrin beta2/beta3 expression was demoted by celastrol, thereby contributing to the inhibition of collagen matrix-SMC interaction. celastrol 80-89 integrin subunit beta 2 Homo sapiens 33-47 22949384-9 2013 The resistin-induced shedding of integrin beta2/beta3 expression was demoted by celastrol, thereby contributing to the inhibition of collagen matrix-SMC interaction. celastrol 80-89 eukaryotic translation elongation factor 1 beta 2 pseudogene 2 Homo sapiens 48-53 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 80-89 toll like receptor 4 Homo sapiens 23-43 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 80-89 toll like receptor 4 Homo sapiens 45-50 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 80-89 toll like receptor 4 Homo sapiens 107-112 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 169-178 toll like receptor 4 Homo sapiens 23-43 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 169-178 toll like receptor 4 Homo sapiens 45-50 22949384-10 2013 Next, resistin-induced Toll-like receptor-4 (TLR-4) expression was abrogated by celastrol, indicating that TLR-4 was the resistin signaling receptor that was blocked by celastrol. celastrol 169-178 toll like receptor 4 Homo sapiens 107-112 23711145-6 2013 Flow cytometry analysis with PI and Annexin V revealed that celastrol induced RA-FLS cell cycle arrest in the G2/M phase and apoptosis. celastrol 60-69 annexin A5 Homo sapiens 36-45 23711145-7 2013 Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. celastrol 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 23711145-7 2013 Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. celastrol 13-22 BCL2 apoptosis regulator Homo sapiens 64-69 23711145-7 2013 Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. celastrol 13-22 caspase 3 Homo sapiens 95-108 23711145-7 2013 Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. celastrol 13-22 collagen type XI alpha 2 chain Homo sapiens 110-114 22954486-0 2012 Celastrol inhibits interleukin-17A-stimulated rheumatoid fibroblast-like synoviocyte migration and invasion through suppression of NF-kappaB-mediated matrix metalloproteinase-9 expression. celastrol 0-9 interleukin 17A Homo sapiens 19-34 23988648-0 2013 miR-224 is critical for celastrol-induced inhibition of migration and invasion of hepatocellular carcinoma cells. celastrol 24-33 microRNA 224 Homo sapiens 0-7 23988648-3 2013 Next, we assessed the effect of celastrol on NF-kappaB transcriptional activity in hepatocellular carcinoma cells using western blot and luciferase reporter assay. celastrol 32-41 nuclear factor kappa B subunit 1 Homo sapiens 45-54 23988648-8 2013 Finally, we evaluated the effect of miR-224 on celastrol-induced anti-tumor activity using miR-224 precursor. celastrol 47-56 microRNA 224 Homo sapiens 36-43 23988648-9 2013 RESULTS: Celastrol significantly impaired migration and invasion of HepG2 cells and inhibited the activation of NF-kappaB and Akt in dose-dependent manner. celastrol 9-18 nuclear factor kappa B subunit 1 Homo sapiens 112-121 23988648-9 2013 RESULTS: Celastrol significantly impaired migration and invasion of HepG2 cells and inhibited the activation of NF-kappaB and Akt in dose-dependent manner. celastrol 9-18 AKT serine/threonine kinase 1 Homo sapiens 126-129 23988648-10 2013 IGF (the strong stimulator of Akt) inhibited the transcriptional activity of NF-kappaB in cells treated with celastrol. celastrol 109-118 AKT serine/threonine kinase 1 Homo sapiens 30-33 23988648-10 2013 IGF (the strong stimulator of Akt) inhibited the transcriptional activity of NF-kappaB in cells treated with celastrol. celastrol 109-118 nuclear factor kappa B subunit 1 Homo sapiens 77-86 23988648-11 2013 Besides, celastrol efficiently decreased the expression of miR-224 and protein expression of MMP-2 and MMP-9. celastrol 9-18 microRNA 224 Homo sapiens 59-66 23988648-11 2013 Besides, celastrol efficiently decreased the expression of miR-224 and protein expression of MMP-2 and MMP-9. celastrol 9-18 matrix metallopeptidase 2 Homo sapiens 93-98 23988648-11 2013 Besides, celastrol efficiently decreased the expression of miR-224 and protein expression of MMP-2 and MMP-9. celastrol 9-18 matrix metallopeptidase 9 Homo sapiens 103-108 23988648-12 2013 ChIP-qPCR showed that p65/NF-kappaB binding to the miR-224 promoter sharply decreased after exposure to celastrol in time-dependent manner. celastrol 104-113 RELA proto-oncogene, NF-kB subunit Homo sapiens 22-25 23988648-12 2013 ChIP-qPCR showed that p65/NF-kappaB binding to the miR-224 promoter sharply decreased after exposure to celastrol in time-dependent manner. celastrol 104-113 nuclear factor kappa B subunit 1 Homo sapiens 26-35 23988648-12 2013 ChIP-qPCR showed that p65/NF-kappaB binding to the miR-224 promoter sharply decreased after exposure to celastrol in time-dependent manner. celastrol 104-113 microRNA 224 Homo sapiens 51-58 23988648-14 2013 Most importantly, miR-224 precursor can reverse the effect of celastrol on impairment of migration and invasion in HepG2 and Huh7 cells. celastrol 62-71 microRNA 224 Homo sapiens 18-25 23988648-15 2013 CONCLUSION: Celastrol treatment inhibits migration and invasion of HCC cell and that the effect is partly due to NF-kappaB regulating miR-224 expression. celastrol 12-21 nuclear factor kappa B subunit 1 Homo sapiens 113-122 23988648-15 2013 CONCLUSION: Celastrol treatment inhibits migration and invasion of HCC cell and that the effect is partly due to NF-kappaB regulating miR-224 expression. celastrol 12-21 microRNA 224 Homo sapiens 134-141 23554889-0 2013 Celastrol suppresses tumor cell growth through targeting an AR-ERG-NF-kappaB pathway in TMPRSS2/ERG fusion gene expressing prostate cancer. celastrol 0-9 ETS transcription factor ERG Homo sapiens 63-66 23554889-0 2013 Celastrol suppresses tumor cell growth through targeting an AR-ERG-NF-kappaB pathway in TMPRSS2/ERG fusion gene expressing prostate cancer. celastrol 0-9 transmembrane serine protease 2 Homo sapiens 88-95 23554889-0 2013 Celastrol suppresses tumor cell growth through targeting an AR-ERG-NF-kappaB pathway in TMPRSS2/ERG fusion gene expressing prostate cancer. celastrol 0-9 ETS transcription factor ERG Homo sapiens 96-99 23554889-8 2013 Our results show Celastrol can significantly inhibit the growth of T/E fusion expressing PCa cells both in vitro and in vivo through targeting three critical signaling pathways: AR, ERG and NF-kB in these cells. celastrol 17-26 ETS transcription factor ERG Homo sapiens 182-185 23065091-0 2012 Celastrol inhibits growth and induces apoptotic cell death in melanoma cells via the activation ROS-dependent mitochondrial pathway and the suppression of PI3K/AKT signaling. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 160-163 23065091-4 2012 Pretreatment with caspase inhibitor modestly attenuated the celastrol-induced increase in PARP cleavage and sub-G1 cell population, implying that caspases play a partial role in celastrol-induced apoptosis. celastrol 60-69 poly (ADP-ribose) polymerase family, member 1 Mus musculus 90-94 23065091-4 2012 Pretreatment with caspase inhibitor modestly attenuated the celastrol-induced increase in PARP cleavage and sub-G1 cell population, implying that caspases play a partial role in celastrol-induced apoptosis. celastrol 178-187 poly (ADP-ribose) polymerase family, member 1 Mus musculus 90-94 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 75-84 B cell leukemia/lymphoma 2 Mus musculus 93-98 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 75-84 BCL2-associated X protein Mus musculus 224-227 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 75-84 B cell leukemia/lymphoma 2 Mus musculus 228-233 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 75-84 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 279-282 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 142-151 B cell leukemia/lymphoma 2 Mus musculus 93-98 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 142-151 BCL2-associated X protein Mus musculus 224-227 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 142-151 B cell leukemia/lymphoma 2 Mus musculus 228-233 23065091-6 2012 Blocking of ROS accumulation with ROS scavengers resulted in inhibition of celastrol-induced Bcl-2 family-mediated apoptosis, indicating that celastrol-induced apoptosis involves ROS generation as well as an increase in the Bax/Bcl-2 ratio leading to release of cytochrome c and AIF. celastrol 142-151 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 279-282 23065091-7 2012 Importantly, silencing of AIF by transfection of siAIF into cells remarkably attenuated celastrol-induced apoptotic cell death. celastrol 88-97 apoptosis-inducing factor, mitochondrion-associated 1 Mus musculus 26-29 23065091-8 2012 Moreover, celastrol inhibited the activation of PI3K/AKT/mTOR signaling cascade in B16 cells. celastrol 10-19 thymoma viral proto-oncogene 1 Mus musculus 53-56 23065091-8 2012 Moreover, celastrol inhibited the activation of PI3K/AKT/mTOR signaling cascade in B16 cells. celastrol 10-19 mechanistic target of rapamycin kinase Mus musculus 57-61 23065091-9 2012 Our data reveal that celastrol inhibits growth and induces apoptosis in melanoma cells via the activation of ROS-mediated caspase-dependent and -independent pathways and the suppression of PI3K/AKT signaling. celastrol 21-30 thymoma viral proto-oncogene 1 Mus musculus 194-197 22954486-0 2012 Celastrol inhibits interleukin-17A-stimulated rheumatoid fibroblast-like synoviocyte migration and invasion through suppression of NF-kappaB-mediated matrix metalloproteinase-9 expression. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 131-140 22954486-0 2012 Celastrol inhibits interleukin-17A-stimulated rheumatoid fibroblast-like synoviocyte migration and invasion through suppression of NF-kappaB-mediated matrix metalloproteinase-9 expression. celastrol 0-9 matrix metallopeptidase 9 Homo sapiens 150-176 22954486-6 2012 Results showed that treatment of RA-FLSs with celastrol suppressed the IL-17A-induced migration and invasion abilities of the cells. celastrol 46-55 interleukin 17A Homo sapiens 71-77 22954486-7 2012 In addition, celastrol inhibited IL-17A-induced matrix metalloproteinase (MMP)-9 mRNA and protein expression, and the proteolytic activity of MMP-9 in RA-FLSs. celastrol 13-22 interleukin 17A Homo sapiens 33-39 22954486-7 2012 In addition, celastrol inhibited IL-17A-induced matrix metalloproteinase (MMP)-9 mRNA and protein expression, and the proteolytic activity of MMP-9 in RA-FLSs. celastrol 13-22 matrix metallopeptidase 9 Homo sapiens 48-80 22954486-7 2012 In addition, celastrol inhibited IL-17A-induced matrix metalloproteinase (MMP)-9 mRNA and protein expression, and the proteolytic activity of MMP-9 in RA-FLSs. celastrol 13-22 matrix metallopeptidase 9 Homo sapiens 142-147 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 matrix metallopeptidase 9 Homo sapiens 91-96 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 nuclear factor kappa B subunit 1 Homo sapiens 139-160 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 nuclear factor kappa B subunit 1 Homo sapiens 162-171 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 matrix metallopeptidase 9 Homo sapiens 180-185 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 NFKB inhibitor alpha Homo sapiens 210-222 22954486-8 2012 Furthermore, our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the binding activity of nuclear factor-kappaB (NF-kappaB) in the MMP-9 promoter, and inhibited IkappaBalpha phosphorylation and nuclear translocation of NF-kappaB. celastrol 39-48 nuclear factor kappa B subunit 1 Homo sapiens 268-277 22954486-9 2012 In conclusion, celastrol can inhibit IL-17A-induced migration and invasion by suppressing NF-kappaB-mediated MMP-9 expression in RA-FLSs. celastrol 15-24 interleukin 17A Homo sapiens 37-43 22954486-9 2012 In conclusion, celastrol can inhibit IL-17A-induced migration and invasion by suppressing NF-kappaB-mediated MMP-9 expression in RA-FLSs. celastrol 15-24 nuclear factor kappa B subunit 1 Homo sapiens 90-99 22954486-9 2012 In conclusion, celastrol can inhibit IL-17A-induced migration and invasion by suppressing NF-kappaB-mediated MMP-9 expression in RA-FLSs. celastrol 15-24 matrix metallopeptidase 9 Homo sapiens 109-114 23272499-0 2012 [Effects of tripterine on NF-kappaB and eotaxin in nasal mucosa of allergic rhinitis rat]. celastrol 12-22 C-C motif chemokine ligand 11 Rattus norvegicus 40-47 23272499-1 2012 OBJECTIVE: To investigate the relationship among the expressions of NF-kappaB, Eotaxin and the effects of tripterine in nasal mucosa of allergic rhinitis rat and to discuss the possible mechanism of tripterine on allergic rhinitis. celastrol 199-209 C-C motif chemokine ligand 11 Rattus norvegicus 79-86 23272499-12 2012 CONCLUSION: Tripterine can inhibit expression of Eotaxin by restraining the activation of NF-kappaB. celastrol 12-22 C-C motif chemokine ligand 11 Rattus norvegicus 49-56 22380712-8 2012 This led to the synthesis of biotinylated celastrols (23 and 24) that were used as affinity reagents in extracts of human Panc-1 cells to identify Annexin II, eEF1A, and beta-tubulin as potential targets of celastrol. celastrol 42-52 annexin A2 Homo sapiens 147-157 22854193-9 2012 Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1alpha, and GRO/KC) as well as cytokines (TNF-alpha and IL-1beta) that induce them, compared to the vehicle-treated rats. celastrol 0-9 C-C motif chemokine ligand 5 Rattus norvegicus 83-89 22854193-9 2012 Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1alpha, and GRO/KC) as well as cytokines (TNF-alpha and IL-1beta) that induce them, compared to the vehicle-treated rats. celastrol 0-9 mast cell protease 1-like 1 Rattus norvegicus 91-96 22854193-9 2012 Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1alpha, and GRO/KC) as well as cytokines (TNF-alpha and IL-1beta) that induce them, compared to the vehicle-treated rats. celastrol 0-9 C-C motif chemokine ligand 3 Rattus norvegicus 98-108 22854193-9 2012 Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1alpha, and GRO/KC) as well as cytokines (TNF-alpha and IL-1beta) that induce them, compared to the vehicle-treated rats. celastrol 0-9 tumor necrosis factor Rattus norvegicus 144-153 22854193-9 2012 Celastrol-treated rats showed a significant reduction in the levels of chemokines (RANTES, MCP-1, MIP-1alpha, and GRO/KC) as well as cytokines (TNF-alpha and IL-1beta) that induce them, compared to the vehicle-treated rats. celastrol 0-9 interleukin 1 beta Rattus norvegicus 158-166 22380712-8 2012 This led to the synthesis of biotinylated celastrols (23 and 24) that were used as affinity reagents in extracts of human Panc-1 cells to identify Annexin II, eEF1A, and beta-tubulin as potential targets of celastrol. celastrol 42-51 annexin A2 Homo sapiens 147-157 22380712-8 2012 This led to the synthesis of biotinylated celastrols (23 and 24) that were used as affinity reagents in extracts of human Panc-1 cells to identify Annexin II, eEF1A, and beta-tubulin as potential targets of celastrol. celastrol 42-51 eukaryotic translation elongation factor 1 alpha 1 Homo sapiens 159-164 22877649-0 2012 Beta-catenin mediates the apoptosis induction effect of celastrol in HT29 cells. celastrol 56-65 catenin beta 1 Homo sapiens 0-12 22877649-1 2012 AIM: We evaluated the apoptosis induction effects of celastrol in human colorectal cancer cell line HT29 in WNT/beta-catenin pathway. celastrol 53-62 catenin beta 1 Homo sapiens 112-124 22877649-7 2012 Celastrol induced HT29 cells apoptosis, and increased the nuclear translocation of beta-catenin. celastrol 0-9 catenin beta 1 Homo sapiens 83-95 22877649-8 2012 Apoptosis induction effects of celastrol were significantly attenuated by beta-catenin siRNA transfection. celastrol 31-40 catenin beta 1 Homo sapiens 74-86 22877649-10 2012 Beta-catenin siRNA significantly inhibited the expression of Bax and Bcl-2 in celastrol-treated HT29 cells. celastrol 78-87 catenin beta 1 Homo sapiens 0-12 22877649-10 2012 Beta-catenin siRNA significantly inhibited the expression of Bax and Bcl-2 in celastrol-treated HT29 cells. celastrol 78-87 BCL2 associated X, apoptosis regulator Homo sapiens 61-64 22877649-10 2012 Beta-catenin siRNA significantly inhibited the expression of Bax and Bcl-2 in celastrol-treated HT29 cells. celastrol 78-87 BCL2 apoptosis regulator Homo sapiens 69-74 22877649-11 2012 SIGNIFICANCE: Beta-catenin mediates the apoptosis induction effects of celastrol in HT29 cells. celastrol 71-80 catenin beta 1 Homo sapiens 14-26 22683631-0 2012 Celastrol inhibits vasculogenesis by suppressing the VEGF-induced functional activity of bone marrow-derived endothelial progenitor cells. celastrol 0-9 vascular endothelial growth factor A Homo sapiens 53-57 22683631-3 2012 The aims of this study are to investigate the effects of Celastrol on VEGF-induced functional activity of BM-EPCs and to identify any mechanisms associated with this process. celastrol 57-66 vascular endothelial growth factor A Homo sapiens 70-74 22683631-4 2012 Here, we show that Celastrol attenuates VEGF secretion in BM-EPCs in vitro. celastrol 19-28 vascular endothelial growth factor A Homo sapiens 40-44 22683631-6 2012 Additionally, Celastrol inhibits the phosphorylation of VEGFR2, endothelial nitric oxide synthase (eNOS), and Akt to attenuate cell functions. celastrol 14-23 kinase insert domain receptor Homo sapiens 56-62 22683631-6 2012 Additionally, Celastrol inhibits the phosphorylation of VEGFR2, endothelial nitric oxide synthase (eNOS), and Akt to attenuate cell functions. celastrol 14-23 nitric oxide synthase 3 Homo sapiens 64-97 22683631-6 2012 Additionally, Celastrol inhibits the phosphorylation of VEGFR2, endothelial nitric oxide synthase (eNOS), and Akt to attenuate cell functions. celastrol 14-23 AKT serine/threonine kinase 1 Homo sapiens 110-113 22683631-7 2012 Taken together, the present study demonstrates that Celastrol decreases Akt/eNOS signaling in BM-EPCs in vitro. celastrol 52-61 AKT serine/threonine kinase 1 Homo sapiens 72-75 22380712-8 2012 This led to the synthesis of biotinylated celastrols (23 and 24) that were used as affinity reagents in extracts of human Panc-1 cells to identify Annexin II, eEF1A, and beta-tubulin as potential targets of celastrol. celastrol 42-52 eukaryotic translation elongation factor 1 alpha 1 Homo sapiens 159-164 22334592-0 2012 Celastrol decreases specificity proteins (Sp) and fibroblast growth factor receptor-3 (FGFR3) in bladder cancer cells. celastrol 0-9 fibroblast growth factor receptor 3 Homo sapiens 50-85 21866552-0 2012 Paraptosis accompanied by autophagy and apoptosis was induced by celastrol, a natural compound with influence on proteasome, ER stress and Hsp90. celastrol 65-74 heat shock protein 90 alpha family class A member 1 Homo sapiens 139-144 21866552-5 2012 Furthermore, MAPK pathways were activated by celastrol and inhibitors of MEK and p38 pathways could prevent the formation of cytoplasmic vacuolization. celastrol 45-54 mitogen-activated protein kinase 14 Homo sapiens 81-84 21866552-10 2012 The potency of celastrol to induce paraptosis, apoptosis and autophagy at the same dose might be related to its capability to affect a variety of pathways including proteasome, ER stress and Hsp90. celastrol 15-24 heat shock protein 90 alpha family class A member 1 Homo sapiens 191-196 22369852-5 2012 We observed that celastrol inhibited both constitutive and inducible STAT3 activation, and the suppression was mediated through the inhibition of activation of upstream kinases c-Src, as well as Janus-activated kinase-1 and -2. celastrol 17-26 signal transducer and activator of transcription 3 Homo sapiens 69-74 22369852-5 2012 We observed that celastrol inhibited both constitutive and inducible STAT3 activation, and the suppression was mediated through the inhibition of activation of upstream kinases c-Src, as well as Janus-activated kinase-1 and -2. celastrol 17-26 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 177-182 22369852-6 2012 Vanadate treatment reversed the celastrol-induced modulation of STAT3, suggesting the involvement of a tyrosine phosphatase. celastrol 32-41 signal transducer and activator of transcription 3 Homo sapiens 64-69 22369852-7 2012 The inhibition of STAT3 activation by celastrol led to the suppression of various gene products involved in proliferation, survival, and angiogenesis. celastrol 38-47 signal transducer and activator of transcription 3 Homo sapiens 18-23 22369852-9 2012 Finally, when administered intraperitoneally, celastrol inhibited STAT3 activation in tumor tissues and the growth of human HCC xenograft tumors in athymic nu/nu mice without any side effects. celastrol 46-55 signal transducer and activator of transcription 3 Homo sapiens 66-71 22369852-0 2012 Celastrol suppresses growth and induces apoptosis of human hepatocellular carcinoma through the modulation of STAT3/JAK2 signaling cascade in vitro and in vivo. celastrol 0-9 signal transducer and activator of transcription 3 Homo sapiens 110-115 22369852-0 2012 Celastrol suppresses growth and induces apoptosis of human hepatocellular carcinoma through the modulation of STAT3/JAK2 signaling cascade in vitro and in vivo. celastrol 0-9 Janus kinase 2 Homo sapiens 116-120 22369852-10 2012 Overall, our results suggest for the first time that celastrol exerts its antiproliferative and proapoptotic effects through suppression of STAT3 signaling in HCC both in vitro and in vivo. celastrol 53-62 signal transducer and activator of transcription 3 Homo sapiens 140-145 22334592-0 2012 Celastrol decreases specificity proteins (Sp) and fibroblast growth factor receptor-3 (FGFR3) in bladder cancer cells. celastrol 0-9 fibroblast growth factor receptor 3 Homo sapiens 87-92 21683142-0 2011 Celastrol regulates innate immunity response via NF-kappaB and Hsp70 in human retinal pigment epithelial cells. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 49-58 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 44-53 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 302-306 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 320-329 activating transcription factor 4 Homo sapiens 145-149 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 320-329 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 206-210 23284992-6 2012 Our findings highlight a novel signaling pathway through which Celastrol increase Noxa expression, and suggest the potential use of ATF4-mediated regulation of Noxa as a promising strategy to improve the anti-cancer activities of ABT-737. celastrol 63-72 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 82-86 22087583-0 2011 Remarkable stereospecific conjugate additions to the Hsp90 inhibitor celastrol. celastrol 69-78 heat shock protein 90 alpha family class A member 1 Homo sapiens 53-58 22087583-1 2011 Celastrol, an important natural product and Hsp90 inhibitor with a wide range of biological and medical activities and broad use as a biological probe, acts by an as yet undetermined mode of action. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 44-49 21951963-7 2011 Celastrol was found to be capable of inducing apoptosis in HaCaT cells as characterized by phosphatidyl-serine (PS) externalization, depolarization of mitochondrial membrane potential and activation of caspase-3. celastrol 0-9 caspase 3 Homo sapiens 202-211 21951963-8 2011 The apoptosis induced by celastrol could be suppressed by Z-IETD-FMK and Z-LEHD-FMK, the respective caspase-8 and caspase-9 inhibitor. celastrol 25-34 caspase 8 Homo sapiens 100-109 21951963-8 2011 The apoptosis induced by celastrol could be suppressed by Z-IETD-FMK and Z-LEHD-FMK, the respective caspase-8 and caspase-9 inhibitor. celastrol 25-34 caspase 9 Homo sapiens 114-123 21951963-9 2011 In addition, western blot analysis revealed a significant augmentation in the protein expression of Bax and attenuation in Bcl-2, suggesting that the celastrol-induced apoptosis acts through both death receptor and mitochondrial pathways. celastrol 150-159 BCL2 associated X, apoptosis regulator Homo sapiens 100-103 21951963-9 2011 In addition, western blot analysis revealed a significant augmentation in the protein expression of Bax and attenuation in Bcl-2, suggesting that the celastrol-induced apoptosis acts through both death receptor and mitochondrial pathways. celastrol 150-159 BCL2 apoptosis regulator Homo sapiens 123-128 21506956-0 2011 Celastrol inhibits proliferation and induces chemosensitization through down-regulation of NF-kappaB and STAT3 regulated gene products in multiple myeloma cells. celastrol 0-9 signal transducer and activator of transcription 3 Homo sapiens 105-110 21506956-2 2011 Thus, in the present study, we investigated whether celastrol could suppress the proliferation and induce chemosensitization of MM cells by interfering with NF-kappaB and STAT3 activation pathways. celastrol 52-61 signal transducer and activator of transcription 3 Homo sapiens 171-176 21506956-7 2011 These effects of celastrol were mediated through suppression of constitutively active NF-kappaB induced by inhibition of IkappaBalpha kinase activation; and the phosphorylation of IkappaBalpha and of p65. celastrol 17-26 NFKB inhibitor alpha Homo sapiens 121-133 21506956-7 2011 These effects of celastrol were mediated through suppression of constitutively active NF-kappaB induced by inhibition of IkappaBalpha kinase activation; and the phosphorylation of IkappaBalpha and of p65. celastrol 17-26 NFKB inhibitor alpha Homo sapiens 180-192 21506956-7 2011 These effects of celastrol were mediated through suppression of constitutively active NF-kappaB induced by inhibition of IkappaBalpha kinase activation; and the phosphorylation of IkappaBalpha and of p65. celastrol 17-26 RELA proto-oncogene, NF-kB subunit Homo sapiens 200-203 21506956-8 2011 Celastrol also inhibited both the constitutive and IL6-induced activation of STAT3, which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3. celastrol 0-9 interleukin 6 Homo sapiens 51-54 21506956-8 2011 Celastrol also inhibited both the constitutive and IL6-induced activation of STAT3, which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3. celastrol 0-9 signal transducer and activator of transcription 3 Homo sapiens 77-82 21506956-8 2011 Celastrol also inhibited both the constitutive and IL6-induced activation of STAT3, which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3. celastrol 0-9 caspase 3 Homo sapiens 260-269 21850367-0 2011 Quinone methide tripterine, celastrol, induces apoptosis in human myeloma cells via NF-kappaB pathway. celastrol 28-37 nuclear factor kappa B subunit 1 Homo sapiens 84-93 21850367-11 2011 In addition, we showed that celastrol induces apoptosis of myeloma cells via activation of the caspase-3 and NF-kappaB pathways. celastrol 28-37 caspase 3 Homo sapiens 95-104 21850367-11 2011 In addition, we showed that celastrol induces apoptosis of myeloma cells via activation of the caspase-3 and NF-kappaB pathways. celastrol 28-37 nuclear factor kappa B subunit 1 Homo sapiens 109-118 22667125-7 2012 The data from in vitro BIAcore analysis showed that the recombinant PSMB1 could bind to celastrol. celastrol 88-97 proteasome 20S subunit beta 1 Homo sapiens 68-73 22667125-8 2012 The binding affinity between PSMB1 and 10 micromol/L celastrol was more than 27RU. celastrol 53-62 proteasome 20S subunit beta 1 Homo sapiens 29-34 23284992-0 2012 Upregulating Noxa by ER stress, celastrol exerts synergistic anti-cancer activity in combination with ABT-737 in human hepatocellular carcinoma cells. celastrol 32-41 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 13-17 23284992-3 2012 The current study demonstrated that combining ABT-737 and Celastrol synergistically suppressed HCC cell proliferation, and induced apoptosis which was accompanied with the activation of caspase cascade and release of cytochrome c from mitochondria. celastrol 58-67 HCC Homo sapiens 95-98 23284992-3 2012 The current study demonstrated that combining ABT-737 and Celastrol synergistically suppressed HCC cell proliferation, and induced apoptosis which was accompanied with the activation of caspase cascade and release of cytochrome c from mitochondria. celastrol 58-67 cytochrome c, somatic Homo sapiens 217-229 23284992-4 2012 Further study revealed that the enhanced Noxa caused by Celastrol was the key factor for the synergy, since small interfering RNA-mediated knockdown of Noxa expression in HCC cells resulted in decreased apoptosis and attenuated anti-proliferative effects of the combination. celastrol 56-65 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 41-45 23284992-4 2012 Further study revealed that the enhanced Noxa caused by Celastrol was the key factor for the synergy, since small interfering RNA-mediated knockdown of Noxa expression in HCC cells resulted in decreased apoptosis and attenuated anti-proliferative effects of the combination. celastrol 56-65 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 152-156 23284992-4 2012 Further study revealed that the enhanced Noxa caused by Celastrol was the key factor for the synergy, since small interfering RNA-mediated knockdown of Noxa expression in HCC cells resulted in decreased apoptosis and attenuated anti-proliferative effects of the combination. celastrol 56-65 HCC Homo sapiens 171-174 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 44-53 activating transcription factor 4 Homo sapiens 145-149 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 44-53 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 206-210 23284992-5 2012 In addition, our study unraveled that, upon Celastrol exposure, the activation of endoplasmic reticulum (ER) stress, specifically, the eIF2alpha-ATF4 pathway played indispensable roles in the activation of Noxa, which was validated by the observation that depletion of ATF4 significantly abrogated the Noxa elevation by Celastrol. celastrol 44-53 activating transcription factor 4 Homo sapiens 269-273 21683142-0 2011 Celastrol regulates innate immunity response via NF-kappaB and Hsp70 in human retinal pigment epithelial cells. celastrol 0-9 heat shock protein family A (Hsp70) member 4 Homo sapiens 63-68 21683142-4 2011 Anti-inflammatory properties of celastrol were determined by measuring expression levels of IL-6 and endogenous NF-kappaB levels during lipopolysaccharide (LPS) exposure by using enzyme-linked immunosorbent assays (ELISA). celastrol 32-41 interleukin 6 Homo sapiens 92-96 21683142-4 2011 Anti-inflammatory properties of celastrol were determined by measuring expression levels of IL-6 and endogenous NF-kappaB levels during lipopolysaccharide (LPS) exposure by using enzyme-linked immunosorbent assays (ELISA). celastrol 32-41 nuclear factor kappa B subunit 1 Homo sapiens 112-121 21683142-7 2011 Simultaneous exposures to LPS and celastrol reduced IL-6 expression levels as well as activity of phosphorylated NF-kappaB at serine 536 (Ser536) in ARPE-19 cells when compared to LPS exposure alone. celastrol 34-43 interleukin 6 Homo sapiens 52-56 21683142-7 2011 Simultaneous exposures to LPS and celastrol reduced IL-6 expression levels as well as activity of phosphorylated NF-kappaB at serine 536 (Ser536) in ARPE-19 cells when compared to LPS exposure alone. celastrol 34-43 nuclear factor kappa B subunit 1 Homo sapiens 113-122 21683142-8 2011 In addition, inhibition of NF-kappaB RelA/p65 activity by celastrol was attenuated when Hsp70 response was silenced by siRNA. celastrol 58-67 nuclear factor kappa B subunit 1 Homo sapiens 27-36 21683142-8 2011 In addition, inhibition of NF-kappaB RelA/p65 activity by celastrol was attenuated when Hsp70 response was silenced by siRNA. celastrol 58-67 RELA proto-oncogene, NF-kB subunit Homo sapiens 42-45 21683142-8 2011 In addition, inhibition of NF-kappaB RelA/p65 activity by celastrol was attenuated when Hsp70 response was silenced by siRNA. celastrol 58-67 heat shock protein family A (Hsp70) member 4 Homo sapiens 88-93 21683142-10 2011 Our findings reveal that celastrol is a novel plant compound which suppresses innate immunity response in human retinal pigment epithelial cells via NF-kappaB and Hsp70 regulation, and that Hsp70 is a critical regulator of NF-kappaB. celastrol 25-34 nuclear factor kappa B subunit 1 Homo sapiens 149-158 21683142-10 2011 Our findings reveal that celastrol is a novel plant compound which suppresses innate immunity response in human retinal pigment epithelial cells via NF-kappaB and Hsp70 regulation, and that Hsp70 is a critical regulator of NF-kappaB. celastrol 25-34 heat shock protein family A (Hsp70) member 4 Homo sapiens 163-168 21683142-10 2011 Our findings reveal that celastrol is a novel plant compound which suppresses innate immunity response in human retinal pigment epithelial cells via NF-kappaB and Hsp70 regulation, and that Hsp70 is a critical regulator of NF-kappaB. celastrol 25-34 heat shock protein family A (Hsp70) member 4 Homo sapiens 190-195 21683142-10 2011 Our findings reveal that celastrol is a novel plant compound which suppresses innate immunity response in human retinal pigment epithelial cells via NF-kappaB and Hsp70 regulation, and that Hsp70 is a critical regulator of NF-kappaB. celastrol 25-34 nuclear factor kappa B subunit 1 Homo sapiens 223-232 21786165-0 2011 Celastrol inhibits tumor cell proliferation and promotes apoptosis through the activation of c-Jun N-terminal kinase and suppression of PI3 K/Akt signaling pathways. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 142-145 21786165-5 2011 Growth inhibitory effects of celastrol correlated with a decrease in the levels of cyclin D1 and cyclin E, but concomitant increase in the levels of p21 and p27. celastrol 29-38 cyclin D1 Homo sapiens 83-92 21786165-6 2011 The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. celastrol 25-34 caspase 3 Homo sapiens 117-126 21786165-5 2011 Growth inhibitory effects of celastrol correlated with a decrease in the levels of cyclin D1 and cyclin E, but concomitant increase in the levels of p21 and p27. celastrol 29-38 H3 histone pseudogene 16 Homo sapiens 149-152 21786165-6 2011 The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. celastrol 25-34 poly(ADP-ribose) polymerase 1 Homo sapiens 139-143 21786165-5 2011 Growth inhibitory effects of celastrol correlated with a decrease in the levels of cyclin D1 and cyclin E, but concomitant increase in the levels of p21 and p27. celastrol 29-38 interferon alpha inducible protein 27 Homo sapiens 157-160 21786165-7 2011 The apoptotic effects of celastrol were preceded by activation of JNK and down-regulation of Akt activation. celastrol 25-34 mitogen-activated protein kinase 8 Homo sapiens 66-69 21786165-7 2011 The apoptotic effects of celastrol were preceded by activation of JNK and down-regulation of Akt activation. celastrol 25-34 AKT serine/threonine kinase 1 Homo sapiens 93-96 21786165-6 2011 The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. celastrol 25-34 caspase 8 Homo sapiens 70-79 21786165-8 2011 JNK was needed for celastrol-induced apoptosis, and inhibition of JNK by pharmacological inhibitor abolished the apoptotic effects. celastrol 19-28 mitogen-activated protein kinase 8 Homo sapiens 0-3 21786165-8 2011 JNK was needed for celastrol-induced apoptosis, and inhibition of JNK by pharmacological inhibitor abolished the apoptotic effects. celastrol 19-28 mitogen-activated protein kinase 8 Homo sapiens 66-69 21786165-6 2011 The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. celastrol 25-34 BH3 interacting domain death agonist Homo sapiens 81-84 21786165-9 2011 Overall, our results indicate that celastrol can inhibit cell proliferation and induce apoptosis through the activation of JNK, suppression of Akt, and down-regulation of anti-apoptotic protein expression. celastrol 35-44 mitogen-activated protein kinase 8 Homo sapiens 123-126 21786165-9 2011 Overall, our results indicate that celastrol can inhibit cell proliferation and induce apoptosis through the activation of JNK, suppression of Akt, and down-regulation of anti-apoptotic protein expression. celastrol 35-44 AKT serine/threonine kinase 1 Homo sapiens 143-146 21786165-6 2011 The apoptosis induced by celastrol was indicated by the activation of caspase-8, bid cleavage, caspase-9 activation, caspase-3 activation, PARP cleavage and through the down regulation of anti-apoptototic proteins. celastrol 25-34 caspase 9 Homo sapiens 95-104 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 1 Homo sapiens 66-70 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 cytochrome b-245 beta chain Homo sapiens 72-76 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 4 Homo sapiens 78-82 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 5 Homo sapiens 87-91 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 1 Homo sapiens 204-208 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 cytochrome b-245 beta chain Homo sapiens 213-217 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 4 Homo sapiens 232-236 21501142-5 2011 KEY RESULTS: Low concentrations of celastrol completely inhibited NOX1, NOX2, NOX4 and NOX5 within minutes with concentration-response curves exhibiting higher Hill coefficients and lower IC50 values for NOX1 and NOX2 compared with NOX4 and NOX5, suggesting differences in their mode of action. celastrol 35-44 NADPH oxidase 5 Homo sapiens 241-245 21501142-6 2011 In a cell-free system, celastrol had an IC50 of 1.24 and 8.4 microM for NOX2 and NOX5, respectively. celastrol 23-32 cytochrome b-245 beta chain Homo sapiens 72-76 21501142-6 2011 In a cell-free system, celastrol had an IC50 of 1.24 and 8.4 microM for NOX2 and NOX5, respectively. celastrol 23-32 NADPH oxidase 5 Homo sapiens 81-85 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 pleckstrin Homo sapiens 33-36 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 pleckstrin Homo sapiens 37-41 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 calcineurin like EF-hand protein 1 Homo sapiens 99-102 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 pleckstrin Homo sapiens 103-107 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 pleckstrin Homo sapiens 33-42 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 NADPH oxidase organizer 1 Homo sapiens 151-156 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 cytochrome b-245 beta chain Homo sapiens 184-188 21501142-8 2011 Celastrol bound to a recombinant p47(phox) and disrupted the binding of the proline rich region of p22(phox) to the tandem SH3 domain of p47(phox) and NOXO1, the cytosolic subunits of NOX2 and NOX1, respectively. celastrol 0-9 NADPH oxidase 1 Homo sapiens 193-197 21501142-9 2011 CONCLUSIONS AND IMPLICATIONS: These results demonstrate that celastrol is a potent inhibitor of NOX enzymes in general with increased potency against NOX1 and NOX2. celastrol 61-70 NADPH oxidase 1 Homo sapiens 150-154 21501142-9 2011 CONCLUSIONS AND IMPLICATIONS: These results demonstrate that celastrol is a potent inhibitor of NOX enzymes in general with increased potency against NOX1 and NOX2. celastrol 61-70 cytochrome b-245 beta chain Homo sapiens 159-163 21466843-9 2011 Celastrol also up-regulated the expression of pro-apoptotic Bax, down-regulated anti-apoptotic Bcl-2, and inhibited Akt phosphorylation. celastrol 0-9 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 21866174-9 2011 HSP32 (also called heme oxygenase-1, HO-1) is the primary mediator of the protective effect of celastrol. celastrol 95-104 heme oxygenase 1 Mus musculus 0-5 21866174-9 2011 HSP32 (also called heme oxygenase-1, HO-1) is the primary mediator of the protective effect of celastrol. celastrol 95-104 heme oxygenase 1 Mus musculus 19-35 21866174-9 2011 HSP32 (also called heme oxygenase-1, HO-1) is the primary mediator of the protective effect of celastrol. celastrol 95-104 heme oxygenase 1 Mus musculus 37-41 21866174-11 2011 Taken together, our data indicate that celastrol inhibits aminoglycoside ototoxicity via HSP32/HO-1 induction. celastrol 39-48 heme oxygenase 1 Mus musculus 89-94 21866174-11 2011 Taken together, our data indicate that celastrol inhibits aminoglycoside ototoxicity via HSP32/HO-1 induction. celastrol 39-48 heme oxygenase 1 Mus musculus 95-99 21466843-9 2011 Celastrol also up-regulated the expression of pro-apoptotic Bax, down-regulated anti-apoptotic Bcl-2, and inhibited Akt phosphorylation. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 95-100 21466843-0 2011 Celastrol induces apoptosis in non-small-cell lung cancer A549 cells through activation of mitochondria- and Fas/FasL-mediated pathways. celastrol 0-9 Fas ligand Homo sapiens 113-117 21466843-6 2011 Celastrol induced A549 cells apoptosis as confirmed by annexin V/propidium iodide staining and DNA fragmentation. celastrol 0-9 annexin A5 Homo sapiens 55-64 21466843-9 2011 Celastrol also up-regulated the expression of pro-apoptotic Bax, down-regulated anti-apoptotic Bcl-2, and inhibited Akt phosphorylation. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 116-119 21466843-7 2011 Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential. celastrol 0-9 caspase 9 Homo sapiens 61-70 21466843-10 2011 These results demonstrate that celastrol can induce apoptosis of human NSCLC A549 cells through activation of both mitochondria- and FasL-mediated pathways. celastrol 31-40 Fas ligand Homo sapiens 133-137 21466843-7 2011 Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential. celastrol 0-9 caspase 8 Homo sapiens 72-81 21569548-13 2011 NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin. celastrol 25-34 heat shock protein 90 alpha family class A member 1 Homo sapiens 55-60 21466843-7 2011 Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential. celastrol 0-9 caspase 3 Homo sapiens 83-92 21466843-7 2011 Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential. celastrol 0-9 collagen type XI alpha 2 chain Homo sapiens 98-102 21466843-7 2011 Celastrol-induced apoptosis was characterized by cleavage of caspase-9, caspase-8, caspase-3, and PARP protein, increased Fas and FasL expression, and a reduction in the mitochondrial membrane potential. celastrol 0-9 Fas ligand Homo sapiens 130-134 21466843-8 2011 Furthermore, celastrol induced the release of cytochrome c. celastrol 13-22 cytochrome c, somatic Homo sapiens 46-58 21569548-9 2011 JNK phosphorylation induced by celastrol was suppressed by NAC and JNK inhibitor SP600125 (SP). celastrol 31-40 mitogen-activated protein kinase 8 Homo sapiens 0-3 21569548-9 2011 JNK phosphorylation induced by celastrol was suppressed by NAC and JNK inhibitor SP600125 (SP). celastrol 31-40 mitogen-activated protein kinase 8 Homo sapiens 67-70 21569548-13 2011 NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin. celastrol 25-34 catalase Homo sapiens 78-86 21569548-10 2011 Moreover, SP significantly inhibited celastrol-induced loss of MMP, cleavage of PARP, caspase 9 and caspase 3, mitochondrial translocation of Bad, cytoplasmic release of cytochrome c, and cell death. celastrol 37-46 collagen type XI alpha 2 chain Homo sapiens 80-84 21569548-13 2011 NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin. celastrol 25-34 thioredoxin Homo sapiens 91-102 21569548-10 2011 Moreover, SP significantly inhibited celastrol-induced loss of MMP, cleavage of PARP, caspase 9 and caspase 3, mitochondrial translocation of Bad, cytoplasmic release of cytochrome c, and cell death. celastrol 37-46 caspase 9 Homo sapiens 86-95 21569548-10 2011 Moreover, SP significantly inhibited celastrol-induced loss of MMP, cleavage of PARP, caspase 9 and caspase 3, mitochondrial translocation of Bad, cytoplasmic release of cytochrome c, and cell death. celastrol 37-46 caspase 3 Homo sapiens 100-109 21569548-10 2011 Moreover, SP significantly inhibited celastrol-induced loss of MMP, cleavage of PARP, caspase 9 and caspase 3, mitochondrial translocation of Bad, cytoplasmic release of cytochrome c, and cell death. celastrol 37-46 cytochrome c, somatic Homo sapiens 170-182 21569548-17 2011 JNK was activated by celastrol-induced ROS accumulation and then initiated mitochondrial-mediated apoptosis. celastrol 21-30 mitogen-activated protein kinase 8 Homo sapiens 0-3 21569548-12 2011 Celastrol downregulated HSP90 client proteins but did not disrupt the interaction between HSP90 and cdc37. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 24-29 21569548-18 2011 Celastrol induced the downregulation of HSP90 client proteins through ROS accumulation and facilitated ROS accumulation by inhibiting MRC complex I activity. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 40-45 21414301-0 2011 Celastrol induces expression of heme oxygenase-1 through ROS/Nrf2/ARE signaling in the HaCaT cells. celastrol 0-9 heme oxygenase 1 Homo sapiens 32-48 21306773-5 2011 Here we exploit a physiological molecular interaction between intercellular adhesion molecule (ICAM)-1 and lymphocyte function associated antigen (LFA)-1 to deliver a potent anti-inflammatory drug, celastrol, specifically and comprehensively to inflamed cells. celastrol 198-207 intercellular adhesion molecule 1 Homo sapiens 62-102 21306773-5 2011 Here we exploit a physiological molecular interaction between intercellular adhesion molecule (ICAM)-1 and lymphocyte function associated antigen (LFA)-1 to deliver a potent anti-inflammatory drug, celastrol, specifically and comprehensively to inflamed cells. celastrol 198-207 integrin subunit alpha L Homo sapiens 107-153 21414301-0 2011 Celastrol induces expression of heme oxygenase-1 through ROS/Nrf2/ARE signaling in the HaCaT cells. celastrol 0-9 NFE2 like bZIP transcription factor 2 Homo sapiens 61-65 21414301-1 2011 We previously demonstrated that celastrol, a quinone methide triterpenoid derived from the medicinal plant Tripterygium wilfordii, exerts its anti-inflammatory activity through up-regulation of heme oxygenase-1 (HO-1) expression in the keratinocytes. celastrol 32-41 heme oxygenase 1 Homo sapiens 194-210 21414301-1 2011 We previously demonstrated that celastrol, a quinone methide triterpenoid derived from the medicinal plant Tripterygium wilfordii, exerts its anti-inflammatory activity through up-regulation of heme oxygenase-1 (HO-1) expression in the keratinocytes. celastrol 32-41 heme oxygenase 1 Homo sapiens 212-216 21414301-2 2011 In this study, we examined the signaling pathways that lead to the up-regulation of HO-1 expression by celastrol. celastrol 103-112 heme oxygenase 1 Homo sapiens 84-88 21414301-3 2011 In HaCaT cells, celastrol-induced HO-1 expression was dependent on ROS generation. celastrol 16-25 heme oxygenase 1 Homo sapiens 34-38 21414301-4 2011 ERK and p38 MAPK were major MAPK pathways responsible for celastrol-induced HO-1 expression. celastrol 58-67 mitogen-activated protein kinase 14 Homo sapiens 8-11 21414301-4 2011 ERK and p38 MAPK were major MAPK pathways responsible for celastrol-induced HO-1 expression. celastrol 58-67 heme oxygenase 1 Homo sapiens 76-80 21414301-5 2011 Celastrol induced Nrf2 activation. celastrol 0-9 NFE2 like bZIP transcription factor 2 Homo sapiens 18-22 21414301-6 2011 Nrf2 knockdown using small interfering RNA (siRNA) inhibited celastrol-induced HO-1 expression. celastrol 61-70 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4 21414301-6 2011 Nrf2 knockdown using small interfering RNA (siRNA) inhibited celastrol-induced HO-1 expression. celastrol 61-70 heme oxygenase 1 Homo sapiens 79-83 21414301-7 2011 Treatment with celastrol resulted in a marked increase in antioxidant response element (ARE)-driven transcriptional activity, which was dependent on ROS generation and activation of ERK and p38 MAPK. celastrol 15-24 mitogen-activated protein kinase 14 Homo sapiens 190-193 21414301-8 2011 Furthermore, Nrf2 siRNA significantly reversed the inhibitory effect of celastrol on IFN-gamma-induced expression of ICAM-1 in the keratinocytes. celastrol 72-81 NFE2 like bZIP transcription factor 2 Homo sapiens 13-17 21414301-8 2011 Furthermore, Nrf2 siRNA significantly reversed the inhibitory effect of celastrol on IFN-gamma-induced expression of ICAM-1 in the keratinocytes. celastrol 72-81 interferon gamma Homo sapiens 85-94 21414301-8 2011 Furthermore, Nrf2 siRNA significantly reversed the inhibitory effect of celastrol on IFN-gamma-induced expression of ICAM-1 in the keratinocytes. celastrol 72-81 intercellular adhesion molecule 1 Homo sapiens 117-123 21414301-9 2011 Taken together, our results indicate that celastrol can activate the ROS-ERK/p38-Nrf2-ARE signaling cascades leading to the up-regulation of HO-1 which is partly responsible for its anti-inflammatory activity in the keratinocytes. celastrol 42-51 mitogen-activated protein kinase 14 Homo sapiens 77-80 21414301-9 2011 Taken together, our results indicate that celastrol can activate the ROS-ERK/p38-Nrf2-ARE signaling cascades leading to the up-regulation of HO-1 which is partly responsible for its anti-inflammatory activity in the keratinocytes. celastrol 42-51 NFE2 like bZIP transcription factor 2 Homo sapiens 81-85 21414301-9 2011 Taken together, our results indicate that celastrol can activate the ROS-ERK/p38-Nrf2-ARE signaling cascades leading to the up-regulation of HO-1 which is partly responsible for its anti-inflammatory activity in the keratinocytes. celastrol 42-51 heme oxygenase 1 Homo sapiens 141-145 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 118-121 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 heme oxygenase 1 Homo sapiens 86-90 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 122-126 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 C-X-C motif chemokine receptor 4 Homo sapiens 128-133 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 inositol-3-phosphate synthase 1 Homo sapiens 92-96 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 notch receptor 1 Homo sapiens 109-116 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 major histocompatibility complex, class II, DR beta 4 Homo sapiens 151-154 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 TNF receptor superfamily member 10b Homo sapiens 159-162 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 DNA damage inducible transcript 3 Homo sapiens 164-168 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 mitogen-activated protein kinase 8 Homo sapiens 170-173 21168266-6 2011 Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported. celastrol 0-9 vascular endothelial growth factor A Homo sapiens 175-179 21425580-5 2011 Moreover, Celastrol decreased the expressions of p-Akt, survivin and Bcl-2 in the Akt signaling pathway. celastrol 10-19 BCL2 apoptosis regulator Homo sapiens 69-74 21159881-9 2011 Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-kappaB activation, indicating this natural compound could be used as a potential therapeutic drug against KSHV malignancies involving vGPCR. celastrol 31-40 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 23-27 21159881-9 2011 Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-kappaB activation, indicating this natural compound could be used as a potential therapeutic drug against KSHV malignancies involving vGPCR. celastrol 31-40 K14 Human gammaherpesvirus 8 51-56 21159881-9 2011 Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-kappaB activation, indicating this natural compound could be used as a potential therapeutic drug against KSHV malignancies involving vGPCR. celastrol 31-40 K14 Human gammaherpesvirus 8 202-207 21249311-0 2011 Enhancement of radiation sensitivity in lung cancer cells by celastrol is mediated by inhibition of Hsp90. celastrol 61-70 heat shock protein 90 alpha family class A member 1 Homo sapiens 100-105 21249311-4 2011 Celastrol inhibited the ATP-binding activity of Hsp90. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 48-53 21249311-5 2011 Furthermore, celastrol treatment dissociated an Hsp90 client protein, EGFR, and this in turn resulted in degradation of the client protein. celastrol 13-22 heat shock protein 90 alpha family class A member 1 Homo sapiens 48-53 21249311-5 2011 Furthermore, celastrol treatment dissociated an Hsp90 client protein, EGFR, and this in turn resulted in degradation of the client protein. celastrol 13-22 epidermal growth factor receptor Homo sapiens 70-74 21249311-7 2011 Moreover celastrol treatment increased p53 levels by phosphorylating Ser15 and Ser20 residues as well as by inhibiting its proteasomal degradation. celastrol 9-18 tumor protein p53 Homo sapiens 39-42 21249311-8 2011 Celastrol may be considered an effective radiosensitizer acting as an inhibitor of Hsp90 and a p53 activator. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 83-88 21249311-8 2011 Celastrol may be considered an effective radiosensitizer acting as an inhibitor of Hsp90 and a p53 activator. celastrol 0-9 tumor protein p53 Homo sapiens 95-98 21134410-6 2011 Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. celastrol 0-9 caspase 7 Homo sapiens 31-52 21134410-6 2011 Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. celastrol 0-9 collagen type XI alpha 2 chain Homo sapiens 54-58 21134410-6 2011 Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. celastrol 0-9 caspase 8 Homo sapiens 69-78 21134410-6 2011 Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. celastrol 0-9 cytochrome c, somatic Homo sapiens 117-129 21134410-6 2011 Celastrol caused activation of caspase-7, -8, and -9, PARP cleavage, caspase-8-mediated bid cleavage, and release of cytochrome c and AIF. celastrol 0-9 apoptosis inducing factor mitochondria associated 1 Homo sapiens 134-137 21134410-7 2011 In addition, celastrol decreased the expression of anti-apoptotic Bcl-2 protein and increased expression of pro-apoptotic Bax protein. celastrol 13-22 BCL2 apoptosis regulator Homo sapiens 66-71 21134410-7 2011 In addition, celastrol decreased the expression of anti-apoptotic Bcl-2 protein and increased expression of pro-apoptotic Bax protein. celastrol 13-22 BCL2 associated X, apoptosis regulator Homo sapiens 122-125 21129982-1 2011 Several Hsp90 modulators have been identified including the N-terminal ligand geldanamycin (GDA), the C-terminal ligand novobiocin (NB), and the co-chaperone disruptor celastrol. celastrol 168-177 heat shock protein 90 alpha family class A member 1 Homo sapiens 8-13 21193311-4 2011 A search for estramustine phosphate analogs led to identification of two triterpenoids, enoxolone, and celastrol, having Shp2 PTP inhibitor activity. celastrol 103-112 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 121-125 21193311-4 2011 A search for estramustine phosphate analogs led to identification of two triterpenoids, enoxolone, and celastrol, having Shp2 PTP inhibitor activity. celastrol 103-112 protein tyrosine phosphatase receptor type U Homo sapiens 126-129 21088503-0 2011 Anticancer activity of Celastrol in combination with ErbB2-targeted therapeutics for treatment of ErbB2-overexpressing breast cancers. celastrol 23-32 erb-b2 receptor tyrosine kinase 2 Homo sapiens 98-103 21088503-3 2011 The triterpene natural product Celastrol inhibits HSP90 and several pathways relevant to ErbB2-dependent oncogenesis including the NFkappaB pathway and the proteasome, and has shown promising activity in other cancer models. celastrol 31-40 heat shock protein 90 alpha family class A member 1 Homo sapiens 50-55 21088503-3 2011 The triterpene natural product Celastrol inhibits HSP90 and several pathways relevant to ErbB2-dependent oncogenesis including the NFkappaB pathway and the proteasome, and has shown promising activity in other cancer models. celastrol 31-40 erb-b2 receptor tyrosine kinase 2 Homo sapiens 89-94 21088503-3 2011 The triterpene natural product Celastrol inhibits HSP90 and several pathways relevant to ErbB2-dependent oncogenesis including the NFkappaB pathway and the proteasome, and has shown promising activity in other cancer models. celastrol 31-40 nuclear factor kappa B subunit 1 Homo sapiens 131-139 21088503-4 2011 Here, we demonstrate that Celastrol exhibits in vitro antitumor activity against a panel of human breast cancer cell lines with selectivity towards those overexpressing ErbB2. celastrol 26-35 erb-b2 receptor tyrosine kinase 2 Homo sapiens 169-174 21088503-5 2011 Celastrol strongly synergized with ErbB2-targeted therapeutics Trastuzumab and Lapatinib, producing higher cytotoxicity with substantially lower doses of Celastrol. celastrol 0-9 erb-b2 receptor tyrosine kinase 2 Homo sapiens 35-40 21088503-5 2011 Celastrol strongly synergized with ErbB2-targeted therapeutics Trastuzumab and Lapatinib, producing higher cytotoxicity with substantially lower doses of Celastrol. celastrol 154-163 erb-b2 receptor tyrosine kinase 2 Homo sapiens 35-40 21088503-6 2011 Celastrol significantly retarded the rate of growth of ErbB2-overexpressing human breast cancer cells in a mouse xenograft model with only minor systemic toxicity. celastrol 0-9 erb-b2 receptor tyrosine kinase 2 Homo sapiens 55-60 21088503-7 2011 Mechanistically, Celastrol not only induced the expected ubiquitinylation and degradation of ErbB2 and other HSP90 client proteins, but it also increased the levels of reactive oxygen species (ROS). celastrol 17-26 erb-b2 receptor tyrosine kinase 2 Homo sapiens 93-98 21088503-7 2011 Mechanistically, Celastrol not only induced the expected ubiquitinylation and degradation of ErbB2 and other HSP90 client proteins, but it also increased the levels of reactive oxygen species (ROS). celastrol 17-26 heat shock protein 90 alpha family class A member 1 Homo sapiens 109-114 21088503-8 2011 Our studies show that the Michael Acceptor functionality in Celastrol is important for its ability to destabilize ErbB2 and exert its bioactivity against ErbB2-overexpressing breast cancer cells. celastrol 60-69 erb-b2 receptor tyrosine kinase 2 Homo sapiens 114-119 21088503-8 2011 Our studies show that the Michael Acceptor functionality in Celastrol is important for its ability to destabilize ErbB2 and exert its bioactivity against ErbB2-overexpressing breast cancer cells. celastrol 60-69 erb-b2 receptor tyrosine kinase 2 Homo sapiens 154-159 21170316-10 2010 In addition, celastrol rapidly blocked cytosolic IkappaBalpha degradation and nuclear translocation of RelA. celastrol 13-22 RELA proto-oncogene, NF-kB subunit Homo sapiens 103-107 20934245-0 2011 Celastrol inhibits the growth of estrogen positive human breast cancer cells through modulation of estrogen receptor alpha. celastrol 0-9 estrogen receptor 1 Homo sapiens 99-122 20934245-4 2011 However, ERalpha regulation by Celastrol has not been reported. celastrol 31-40 estrogen receptor 1 Homo sapiens 9-16 20934245-6 2011 We observed that Celastrol decreased expression of ERalpha at both the mRNA and the protein levels in MCF7 and T47D human breast cancer cells. celastrol 17-26 estrogen receptor 1 Homo sapiens 51-58 20934245-7 2011 Results from a luciferase assay showed that Celastrol decreased the transcriptional activity of ERalpha. celastrol 44-53 estrogen receptor 1 Homo sapiens 96-103 20934245-8 2011 Also, Celastrol treatment inhibited ERalpha target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. celastrol 6-15 estrogen receptor 1 Homo sapiens 36-43 20934245-8 2011 Also, Celastrol treatment inhibited ERalpha target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. celastrol 6-15 cyclin D1 Homo sapiens 93-104 20934245-8 2011 Also, Celastrol treatment inhibited ERalpha target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. celastrol 6-15 progesterone receptor Homo sapiens 106-127 20934245-8 2011 Also, Celastrol treatment inhibited ERalpha target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. celastrol 6-15 progesterone receptor Homo sapiens 129-131 20934245-8 2011 Also, Celastrol treatment inhibited ERalpha target gene expression, including expressions of cyclin D(1), progesterone receptor (PR), and c-Myb leading to cell cycle arrest and growth inhibition of breast cancer cells. celastrol 6-15 MYB proto-oncogene, transcription factor Homo sapiens 138-143 20934245-9 2011 We propose that Celastrol, an anti-cancer drug extracted from natural sources, induces inhibition of cell growth through modulation of ERalpha in estrogen positive breast cancer cells and is a candidate for use in cancer chemotherapy for human breast cancer. celastrol 16-25 estrogen receptor 1 Homo sapiens 135-142 21865725-0 2011 Celastrol inhibits breast cancer cell invasion via suppression of NF-kB-mediated matrix metalloproteinase-9 expression. celastrol 0-9 matrix metallopeptidase 9 Homo sapiens 81-107 21865725-6 2011 We also found that celastrol inhibited PMA-induced MMP-9 expression at both the mRNA and the protein levels, and the proteolytic activity of MMP-9 in MCF-7 cells. celastrol 19-28 matrix metallopeptidase 9 Homo sapiens 51-56 21865725-6 2011 We also found that celastrol inhibited PMA-induced MMP-9 expression at both the mRNA and the protein levels, and the proteolytic activity of MMP-9 in MCF-7 cells. celastrol 19-28 matrix metallopeptidase 9 Homo sapiens 141-146 21865725-7 2011 Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-kappaB in the MMP-9 promoter, and inhibited degradation of IkappaBalpha and nuclear translocation of NF-kappaB. celastrol 26-35 matrix metallopeptidase 9 Homo sapiens 78-83 21865725-7 2011 Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-kappaB in the MMP-9 promoter, and inhibited degradation of IkappaBalpha and nuclear translocation of NF-kappaB. celastrol 26-35 nuclear factor kappa B subunit 1 Homo sapiens 130-139 21865725-7 2011 Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-kappaB in the MMP-9 promoter, and inhibited degradation of IkappaBalpha and nuclear translocation of NF-kappaB. celastrol 26-35 matrix metallopeptidase 9 Homo sapiens 147-152 21865725-7 2011 Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-kappaB in the MMP-9 promoter, and inhibited degradation of IkappaBalpha and nuclear translocation of NF-kappaB. celastrol 26-35 NFKB inhibitor alpha Homo sapiens 192-204 21865725-7 2011 Our results revealed that celastrol inhibited the transcriptional activity of MMP-9 by suppression of the DNA binding activity of NF-kappaB in the MMP-9 promoter, and inhibited degradation of IkappaBalpha and nuclear translocation of NF-kappaB. celastrol 26-35 nuclear factor kappa B subunit 1 Homo sapiens 234-243 21865725-8 2011 CONCLUSION: These results indicate that celastrol inhibits NF-kappaB-mediated MMP-9 expression, resulting in suppression of breast cancer cell invasion and migration that is induced by PMA. celastrol 40-49 nuclear factor kappa B subunit 1 Homo sapiens 59-68 21865725-8 2011 CONCLUSION: These results indicate that celastrol inhibits NF-kappaB-mediated MMP-9 expression, resulting in suppression of breast cancer cell invasion and migration that is induced by PMA. celastrol 40-49 matrix metallopeptidase 9 Homo sapiens 78-83 21170316-6 2010 We found that celastrol inhibited cell proliferation in all three AIPC cell lines (PC-3, DU145 and CL1), with IC50 in the range of 1-2 microM. celastrol 14-23 adhesion G protein-coupled receptor L1 Homo sapiens 99-102 21170316-8 2010 Celastrol significantly induced apoptosis as evidenced by increased sub-G1 population, caspase activation and PARP cleavage. celastrol 0-9 collagen type XI alpha 2 chain Homo sapiens 110-114 21170316-9 2010 Moreover, celastrol promoted cleavage of the anti-apoptotic protein Mcl-1 and activated the pro-apoptotic protein Noxa. celastrol 10-19 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 68-73 21170316-10 2010 In addition, celastrol rapidly blocked cytosolic IkappaBalpha degradation and nuclear translocation of RelA. celastrol 13-22 NFKB inhibitor alpha Homo sapiens 49-61 21170316-11 2010 Likewise, celastrol inhibited the expression of multiple NF-kappaB target genes that are involved in proliferation, invasion and anti-apoptosis. celastrol 10-19 nuclear factor kappa B subunit 1 Homo sapiens 57-66 21170316-14 2010 CONCLUSIONS/SIGNIFICANCE: Our data suggest that, via targeting the proteasome, celastrol suppresses proliferation, invasion and angiogenesis by inducing the apoptotic machinery and attenuating constitutive NF-kappaB activity in AIPC both in vitro and in vivo. celastrol 79-88 nuclear factor kappa B subunit 1 Homo sapiens 206-215 21170316-0 2010 Natural proteasome inhibitor celastrol suppresses androgen-independent prostate cancer progression by modulating apoptotic proteins and NF-kappaB. celastrol 29-38 nuclear factor kappa B subunit 1 Homo sapiens 136-145 21170316-1 2010 BACKGROUND: Celastrol is a natural proteasome inhibitor that exhibits promising anti-tumor effects in human malignancies, especially the androgen-independent prostate cancer (AIPC) with constitutive NF-kappaB activation. celastrol 12-21 nuclear factor kappa B subunit 1 Homo sapiens 199-208 21170316-4 2010 In the current study, we aim to test the hypothesis that celastrol suppresses AIPC progression via inhibiting the constitutive NF-kappaB activity as well as modulating the Bcl-2 family proteins. celastrol 57-66 nuclear factor kappa B subunit 1 Homo sapiens 127-136 20605676-0 2010 Up-regulation of death receptor 4 and 5 by celastrol enhances the anti-cancer activity of TRAIL/Apo-2L. celastrol 43-52 TNF receptor superfamily member 10a Homo sapiens 17-33 20798912-0 2010 Celastrol suppresses invasion of colon and pancreatic cancer cells through the downregulation of expression of CXCR4 chemokine receptor. celastrol 0-9 C-X-C motif chemokine receptor 4 Homo sapiens 111-116 20798912-0 2010 Celastrol suppresses invasion of colon and pancreatic cancer cells through the downregulation of expression of CXCR4 chemokine receptor. celastrol 0-9 C-X-C motif chemokine receptor 4 Homo sapiens 117-135 20798912-3 2010 In the current report, we demonstrate that celastrol can downregulate the CXCR4 expression on breast cancer MCF-7 cells stably transfected with HER2, an oncogene known to induce the chemokine receptor. celastrol 43-52 C-X-C motif chemokine receptor 4 Homo sapiens 74-79 20798912-3 2010 In the current report, we demonstrate that celastrol can downregulate the CXCR4 expression on breast cancer MCF-7 cells stably transfected with HER2, an oncogene known to induce the chemokine receptor. celastrol 43-52 erb-b2 receptor tyrosine kinase 2 Homo sapiens 144-148 20798912-3 2010 In the current report, we demonstrate that celastrol can downregulate the CXCR4 expression on breast cancer MCF-7 cells stably transfected with HER2, an oncogene known to induce the chemokine receptor. celastrol 43-52 C-X-C motif chemokine receptor 4 Homo sapiens 182-200 20798912-6 2010 Quantitative reverse transcription polymerase chain reaction analysis revealed that downregulation of CXCR4 messenger RNA (mRNA) by celastrol occurred at the translational level. celastrol 132-141 C-X-C motif chemokine receptor 4 Homo sapiens 102-107 20798912-8 2010 Abrogation of the chemokine receptor by celastrol or by gene-silencing was accompanied by suppression of invasiveness of colon cancer cells induced by CXCL12, the ligand for CXCR4. celastrol 40-49 C-X-C motif chemokine receptor 4 Homo sapiens 18-36 20798912-8 2010 Abrogation of the chemokine receptor by celastrol or by gene-silencing was accompanied by suppression of invasiveness of colon cancer cells induced by CXCL12, the ligand for CXCR4. celastrol 40-49 C-X-C motif chemokine ligand 12 Homo sapiens 151-157 20798912-8 2010 Abrogation of the chemokine receptor by celastrol or by gene-silencing was accompanied by suppression of invasiveness of colon cancer cells induced by CXCL12, the ligand for CXCR4. celastrol 40-49 C-X-C motif chemokine receptor 4 Homo sapiens 174-179 20798912-9 2010 This effect was not cell type-specific as celastrol also abolished invasiveness of pancreatic tumor cells, and this effect again correlated with the disappearance of both the CXCR4 mRNA and CXCR4 protein. celastrol 42-51 C-X-C motif chemokine receptor 4 Homo sapiens 175-180 20798912-9 2010 This effect was not cell type-specific as celastrol also abolished invasiveness of pancreatic tumor cells, and this effect again correlated with the disappearance of both the CXCR4 mRNA and CXCR4 protein. celastrol 42-51 C-X-C motif chemokine receptor 4 Homo sapiens 190-195 20798912-11 2010 Overall, these results show that celastrol has potential in suppressing invasion and metastasis of cancer cells by down-modulation of CXCR4 expression. celastrol 33-42 C-X-C motif chemokine receptor 4 Homo sapiens 134-139 20605676-5 2010 Taken together, the present study demonstrates that the enhanced mRNA and protein expression of DR4 and DR5 play prominent roles in the sensitization of celastrol to TRAIL/Apo-2L-induced apoptosis, in a p38 MAPK-independent manner. celastrol 153-162 TNF receptor superfamily member 10a Homo sapiens 96-99 20605676-5 2010 Taken together, the present study demonstrates that the enhanced mRNA and protein expression of DR4 and DR5 play prominent roles in the sensitization of celastrol to TRAIL/Apo-2L-induced apoptosis, in a p38 MAPK-independent manner. celastrol 153-162 TNF receptor superfamily member 10b Homo sapiens 104-107 20605676-5 2010 Taken together, the present study demonstrates that the enhanced mRNA and protein expression of DR4 and DR5 play prominent roles in the sensitization of celastrol to TRAIL/Apo-2L-induced apoptosis, in a p38 MAPK-independent manner. celastrol 153-162 TNF superfamily member 10 Homo sapiens 172-178 20605676-0 2010 Up-regulation of death receptor 4 and 5 by celastrol enhances the anti-cancer activity of TRAIL/Apo-2L. celastrol 43-52 TNF superfamily member 10 Homo sapiens 96-102 20605676-5 2010 Taken together, the present study demonstrates that the enhanced mRNA and protein expression of DR4 and DR5 play prominent roles in the sensitization of celastrol to TRAIL/Apo-2L-induced apoptosis, in a p38 MAPK-independent manner. celastrol 153-162 mitogen-activated protein kinase 14 Homo sapiens 203-206 20605676-1 2010 Our previous study demonstrated that celastrol combined with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo-2L) exhibited significant synergistic anti-cancer activities, thus we were promoted to investigate the molecular mechanism of this synergy. celastrol 37-46 TNF superfamily member 10 Homo sapiens 124-130 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF receptor superfamily member 10a Homo sapiens 56-72 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF receptor superfamily member 10a Homo sapiens 74-77 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF receptor superfamily member 10b Homo sapiens 86-89 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF receptor superfamily member 10a Homo sapiens 183-186 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF receptor superfamily member 10b Homo sapiens 191-194 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 collagen type XI alpha 2 chain Homo sapiens 239-243 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 33-42 TNF superfamily member 10 Homo sapiens 302-308 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 282-291 TNF receptor superfamily member 10a Homo sapiens 56-72 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 282-291 TNF receptor superfamily member 10a Homo sapiens 74-77 20605676-2 2010 Here in this study, we show that celastrol up-regulates death receptor 4 (DR4) and 5 (DR5) expression at mRNA, total protein and cell surface levels, and the specific knockdown using DR4- or DR5-targeting siRNA transfection attenuates the PARP cleavage caused by the combination of celastrol and TRAIL/Apo-2L, denoting the critical roles of DR induction in this sensitization. celastrol 282-291 TNF receptor superfamily member 10b Homo sapiens 86-89 20605676-3 2010 Of note is that although celastrol activates p38 mitogen activated protein kinases (p38 MAPK), SB203580, one specific inhibitor of p38, fails to interrupt celastrol-induced DR4 expression and the enhanced apoptosis caused by celastrol plus TRAIL/Apo-2L. celastrol 25-34 mitogen-activated protein kinase 14 Homo sapiens 45-48 20480272-0 2010 Celastrol regulates multiple nuclear transcription factors belonging to HSP90"s clients in a dose- and cell type-dependent way. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 72-77 20480272-1 2010 Celastrol, a novel HSP90 inhibitor, has recently attracted much attention due to its potential in multiple applications, such as anti-inflammation use, degenerative neuron disease relief, and tumor management. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 19-24 20480272-2 2010 At present, the studies in celastrol"s effects on HSP90"s clients have focused on the kinase sub-population, while another key sub-population, nuclear transcription factors (TFs), is not being well-explored. celastrol 27-36 heat shock protein 90 alpha family class A member 1 Homo sapiens 50-55 20480272-3 2010 In this study, we observe the effects of celastrol on 18 TFs (belonging to HSP90 clients) in three human cell lines: MCF-7 (breast cancer), HepG2 (hepatoma), and THP-1 (monocytic leukemia). celastrol 41-50 heat shock protein 90 alpha family class A member 1 Homo sapiens 75-80 20480272-6 2010 Celastrol"s capability to affect multiple TFs was consistent with its altering HSP90/TFs interactions and disrupting HSP90/Hop interaction, in addition to the reported damaging HSP90/Cdc37 interaction. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 79-84 20480272-6 2010 Celastrol"s capability to affect multiple TFs was consistent with its altering HSP90/TFs interactions and disrupting HSP90/Hop interaction, in addition to the reported damaging HSP90/Cdc37 interaction. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 117-122 20480272-6 2010 Celastrol"s capability to affect multiple TFs was consistent with its altering HSP90/TFs interactions and disrupting HSP90/Hop interaction, in addition to the reported damaging HSP90/Cdc37 interaction. celastrol 0-9 stress induced phosphoprotein 1 Homo sapiens 123-126 20480272-6 2010 Celastrol"s capability to affect multiple TFs was consistent with its altering HSP90/TFs interactions and disrupting HSP90/Hop interaction, in addition to the reported damaging HSP90/Cdc37 interaction. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 117-122 20480272-6 2010 Celastrol"s capability to affect multiple TFs was consistent with its altering HSP90/TFs interactions and disrupting HSP90/Hop interaction, in addition to the reported damaging HSP90/Cdc37 interaction. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 183-188 20480272-7 2010 This work confirms, for the first time, that celastrol has broad effects on TFs belonging to HSP90"s clients, casts new light on understanding these reported actions, and suggests new possible applications for celastrol, such as diabetes management. celastrol 45-54 heat shock protein 90 alpha family class A member 1 Homo sapiens 93-98 20647545-6 2010 Although parthenolide and BMS-345541 had no inhibitory effects on osteoblast function, celastrol prevented IL1beta-induced TAK1 activation and inhibited osteoblast growth, differentiation, and bone nodule formation. celastrol 87-96 interleukin 1 beta Homo sapiens 107-114 20647545-6 2010 Although parthenolide and BMS-345541 had no inhibitory effects on osteoblast function, celastrol prevented IL1beta-induced TAK1 activation and inhibited osteoblast growth, differentiation, and bone nodule formation. celastrol 87-96 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 123-127 20599745-8 2010 These results suggest that celastrol may exert anti-inflammatory responses by suppressing IFN-gamma-induced expression of ICAM-1 and subsequent monocyte adhesion via expression of HO-1 in the keratinocytes. celastrol 27-36 interferon gamma Homo sapiens 90-99 20414191-0 2010 Celastrol attenuates hypertension-induced inflammation and oxidative stress in vascular smooth muscle cells via induction of heme oxygenase-1. celastrol 0-9 heme oxygenase 1 Rattus norvegicus 125-141 20414191-11 2010 Celastrol also blocked activation of extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and Akt signaling both in vivo and in vitro. celastrol 0-9 Eph receptor B1 Rattus norvegicus 37-74 20414191-11 2010 Celastrol also blocked activation of extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and Akt signaling both in vivo and in vitro. celastrol 0-9 Eph receptor B1 Rattus norvegicus 76-79 20414191-12 2010 More importantly, celastrol increased heme oxygenase-1 (HO-1) expression and activity, whereas zinc protoporphyrin 9 (ZnPP9), a HO-1 inhibitor, partially abolished the beneficial effects of celastrol on hypertensive rats and VSMCs. celastrol 18-27 heme oxygenase 1 Rattus norvegicus 38-54 20472666-0 2010 Celastrol acts as a potent antimetastatic agent targeting beta1 integrin and inhibiting cell-extracellular matrix adhesion, in part via the p38 mitogen-activated protein kinase pathway. celastrol 0-9 mitogen-activated protein kinase 14 Mus musculus 140-143 20472666-6 2010 In understanding the underlying mechanisms, we found that celastrol activated p38 mitogen-activated protein kinase (MAPK) by phosphorylation before the decrement of phosphorylated FAK and that this action was independent of the presence of fibronectin. celastrol 58-67 mitogen-activated protein kinase 14 Mus musculus 78-81 20472666-6 2010 In understanding the underlying mechanisms, we found that celastrol activated p38 mitogen-activated protein kinase (MAPK) by phosphorylation before the decrement of phosphorylated FAK and that this action was independent of the presence of fibronectin. celastrol 58-67 PTK2 protein tyrosine kinase 2 Mus musculus 180-183 20472666-6 2010 In understanding the underlying mechanisms, we found that celastrol activated p38 mitogen-activated protein kinase (MAPK) by phosphorylation before the decrement of phosphorylated FAK and that this action was independent of the presence of fibronectin. celastrol 58-67 fibronectin 1 Mus musculus 240-251 20472666-10 2010 Taken together, these data demonstrate for the first time that celastrol exerts potent antimetastatic activity both in vitro and in vivo, and they provide new evidence for the critical roles of p38 MAPK in the regulation of integrin function and cell adhesion. celastrol 63-72 mitogen-activated protein kinase 14 Mus musculus 194-202 20599745-0 2010 Celastrol suppresses IFN-gamma-induced ICAM-1 expression and subsequent monocyte adhesiveness via the induction of heme oxygenase-1 in the HaCaT cells. celastrol 0-9 interferon gamma Homo sapiens 21-30 20599745-0 2010 Celastrol suppresses IFN-gamma-induced ICAM-1 expression and subsequent monocyte adhesiveness via the induction of heme oxygenase-1 in the HaCaT cells. celastrol 0-9 intercellular adhesion molecule 1 Homo sapiens 39-45 20599745-0 2010 Celastrol suppresses IFN-gamma-induced ICAM-1 expression and subsequent monocyte adhesiveness via the induction of heme oxygenase-1 in the HaCaT cells. celastrol 0-9 heme oxygenase 1 Homo sapiens 115-131 20599745-2 2010 In this study, we examined the suppressive effect of celastrol on IFN-gamma-induced expression of ICAM-1 and the molecular mechanism responsible for these activities. celastrol 53-62 interferon gamma Homo sapiens 66-75 20599745-2 2010 In this study, we examined the suppressive effect of celastrol on IFN-gamma-induced expression of ICAM-1 and the molecular mechanism responsible for these activities. celastrol 53-62 intercellular adhesion molecule 1 Homo sapiens 98-104 20599745-3 2010 We found that celastrol induced mRNA and protein expression of heme oxygenase-1 (HO-1) in the human keratinocyte cell line HaCaT. celastrol 14-23 heme oxygenase 1 Homo sapiens 63-79 20599745-3 2010 We found that celastrol induced mRNA and protein expression of heme oxygenase-1 (HO-1) in the human keratinocyte cell line HaCaT. celastrol 14-23 heme oxygenase 1 Homo sapiens 81-85 20599745-4 2010 Treatment of HaCaT cells with tin protoporphyrin IX (SnPP), a specific inhibitor of HO-1, reversed the suppressive effect of celastrol on IFN-gamma-induced protein and mRNA expression of ICAM-1. celastrol 125-134 heme oxygenase 1 Homo sapiens 84-88 20599745-4 2010 Treatment of HaCaT cells with tin protoporphyrin IX (SnPP), a specific inhibitor of HO-1, reversed the suppressive effect of celastrol on IFN-gamma-induced protein and mRNA expression of ICAM-1. celastrol 125-134 interferon gamma Homo sapiens 138-147 20599745-4 2010 Treatment of HaCaT cells with tin protoporphyrin IX (SnPP), a specific inhibitor of HO-1, reversed the suppressive effect of celastrol on IFN-gamma-induced protein and mRNA expression of ICAM-1. celastrol 125-134 intercellular adhesion molecule 1 Homo sapiens 187-193 20599745-5 2010 HO-1 knockdown using small interfering RNA (siRNA) led to reverse inhibition of IFN-gamma-induced up-regulation of ICAM-1 by celastrol. celastrol 125-134 heme oxygenase 1 Homo sapiens 0-4 20957029-6 2010 Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator. celastrol 45-54 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 23-26 20957029-6 2010 Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator. celastrol 45-54 heat shock protein family A (Hsp70) member 4 Homo sapiens 71-76 20957029-6 2010 Heat stress- and other HSP inducer (CdCl(2), celastrol, MG132)-induced HSP70 expression could be inhibited by AICAR, an AMPK specific activator. celastrol 45-54 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 110-115 20723296-0 2010 [Celastrol down-regulates expression of P-Akt and cyclin D1 in HL-60 cells and induces apoptosis]. celastrol 1-10 cyclin D1 Homo sapiens 50-59 20723296-5 2010 The Celastrol suppressed the expression of pAkt and Cyclin D1 in HL-60 cells to a varying degree which showed obvious concentration-and time-dependent manners. celastrol 4-13 cyclin D1 Homo sapiens 52-61 20599745-5 2010 HO-1 knockdown using small interfering RNA (siRNA) led to reverse inhibition of IFN-gamma-induced up-regulation of ICAM-1 by celastrol. celastrol 125-134 interferon gamma Homo sapiens 80-89 20599745-5 2010 HO-1 knockdown using small interfering RNA (siRNA) led to reverse inhibition of IFN-gamma-induced up-regulation of ICAM-1 by celastrol. celastrol 125-134 intercellular adhesion molecule 1 Homo sapiens 115-121 20599745-8 2010 These results suggest that celastrol may exert anti-inflammatory responses by suppressing IFN-gamma-induced expression of ICAM-1 and subsequent monocyte adhesion via expression of HO-1 in the keratinocytes. celastrol 27-36 intercellular adhesion molecule 1 Homo sapiens 122-128 20599745-6 2010 In addition, SnPP reversed suppression of IFN-gamma-induced promoter activity of ICAM-1 by celastrol. celastrol 91-100 interferon gamma Homo sapiens 42-51 20599745-6 2010 In addition, SnPP reversed suppression of IFN-gamma-induced promoter activity of ICAM-1 by celastrol. celastrol 91-100 intercellular adhesion molecule 1 Homo sapiens 81-87 20599745-8 2010 These results suggest that celastrol may exert anti-inflammatory responses by suppressing IFN-gamma-induced expression of ICAM-1 and subsequent monocyte adhesion via expression of HO-1 in the keratinocytes. celastrol 27-36 heme oxygenase 1 Homo sapiens 180-184 20599745-7 2010 Furthermore, blockage of HO-1 activity by SnPP and HO-1 siRNA reversed the inhibitory effect of celastrol on IFN-gamma-induced adhesion of monocytes to keratinocytes. celastrol 96-105 heme oxygenase 1 Homo sapiens 25-29 20599745-7 2010 Furthermore, blockage of HO-1 activity by SnPP and HO-1 siRNA reversed the inhibitory effect of celastrol on IFN-gamma-induced adhesion of monocytes to keratinocytes. celastrol 96-105 heme oxygenase 1 Homo sapiens 51-55 20188206-6 2010 Celastrol-induced HSP accumulation was mediated by HSF1-DNA binding activity since this response was inhibited by the HSF1 activation inhibitor, KNK437. celastrol 0-9 heat shock 70kDa protein L homeolog Xenopus laevis 18-21 20599745-7 2010 Furthermore, blockage of HO-1 activity by SnPP and HO-1 siRNA reversed the inhibitory effect of celastrol on IFN-gamma-induced adhesion of monocytes to keratinocytes. celastrol 96-105 interferon gamma Homo sapiens 109-118 20188206-0 2010 Celastrol can inhibit proteasome activity and upregulate the expression of heat shock protein genes, hsp30 and hsp70, in Xenopus laevis A6 cells. celastrol 0-9 heat shock 70kDa protein L homeolog Xenopus laevis 75-93 20188206-0 2010 Celastrol can inhibit proteasome activity and upregulate the expression of heat shock protein genes, hsp30 and hsp70, in Xenopus laevis A6 cells. celastrol 0-9 heat shock protein 30E L homeolog Xenopus laevis 101-106 20188206-0 2010 Celastrol can inhibit proteasome activity and upregulate the expression of heat shock protein genes, hsp30 and hsp70, in Xenopus laevis A6 cells. celastrol 0-9 heat shock 70kDa protein L homeolog Xenopus laevis 111-116 20188206-6 2010 Celastrol-induced HSP accumulation was mediated by HSF1-DNA binding activity since this response was inhibited by the HSF1 activation inhibitor, KNK437. celastrol 0-9 heat shock factor protein Xenopus laevis 51-55 20188206-6 2010 Celastrol-induced HSP accumulation was mediated by HSF1-DNA binding activity since this response was inhibited by the HSF1 activation inhibitor, KNK437. celastrol 0-9 heat shock factor protein Xenopus laevis 118-122 20188206-7 2010 Simultaneous exposure of cells with celastrol plus either mild heat shock or the proteasome inhibitor, MG132, produced an enhanced accumulation of HSP30 that was greater than the sum of the individual stressors alone. celastrol 36-45 heat shock protein 30E L homeolog Xenopus laevis 147-152 20188206-3 2010 In this study, we show that celastrol, a quinone methide triterpene and anti-inflammatory agent, inhibited proteasome activity and enhanced HSP accumulation in Xenopus laevis A6 kidney epithelial cells. celastrol 28-37 heat shock 70kDa protein L homeolog Xenopus laevis 140-143 20188206-8 2010 Immunocytochemical analysis revealed that celastrol-induced HSP30 accumulation occurred in the cytoplasm in a granular pattern supplemented with larger circular HSP30 staining structures. celastrol 42-51 heat shock protein 30E L homeolog Xenopus laevis 60-65 20188206-8 2010 Immunocytochemical analysis revealed that celastrol-induced HSP30 accumulation occurred in the cytoplasm in a granular pattern supplemented with larger circular HSP30 staining structures. celastrol 42-51 heat shock protein 30E L homeolog Xenopus laevis 161-166 20188206-11 2010 In conclusion, this study has shown that celastrol inhibited proteasome activity and induced HSF1-mediated expression of hsp genes in amphibian cells. celastrol 41-50 heat shock factor protein Xenopus laevis 93-97 20188206-11 2010 In conclusion, this study has shown that celastrol inhibited proteasome activity and induced HSF1-mediated expression of hsp genes in amphibian cells. celastrol 41-50 heat shock 70kDa protein L homeolog Xenopus laevis 121-124 20154087-8 2010 We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL. celastrol 111-120 DNA damage inducible transcript 3 Homo sapiens 143-147 20398364-0 2010 HSP90 inhibitor, celastrol, arrests human monocytic leukemia cell U937 at G0/G1 in thiol-containing agents reversible way. celastrol 17-26 heat shock protein 90 alpha family class A member 1 Homo sapiens 0-5 20398364-2 2010 Recently, celastrol is identified both as a novel inhibitor of HSP90 and as a potential anti-tumor agent. celastrol 10-19 heat shock protein 90 alpha family class A member 1 Homo sapiens 63-68 20398364-8 2010 CONCLUSIONS: Our results disclose a novel action of celastrol-- causing cell cycle arrest at G0/G1 phase based upon thiol-related HSP90 inhibition. celastrol 52-61 heat shock protein 90 alpha family class A member 1 Homo sapiens 130-135 20154087-0 2010 Celastrol, a triterpene, enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and up-regulation of death receptors. celastrol 0-9 TNF superfamily member 10 Homo sapiens 34-39 20154087-1 2010 Whether celastrol, a triterpene from traditional Chinese medicine, can modulate the anticancer effects of TRAIL, the cytokine that is currently in clinical trial, was investigated. celastrol 8-17 TNF superfamily member 10 Homo sapiens 106-111 20154087-8 2010 We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL. celastrol 111-120 TNF receptor superfamily member 10b Homo sapiens 152-155 20154087-2 2010 As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells. celastrol 171-180 caspase 8 Homo sapiens 134-143 20226165-4 2010 Celastrol (i) inhibits directly the IKKalpha and beta kinases, (ii) inactivates the Cdc37 and p23 proteins which are co-chaperones of HSP90, (iii) inhibits the function of proteasomes, and (iv) activates the HSF1 and subsequently triggers the heat shock response. celastrol 0-9 component of inhibitor of nuclear factor kappa B kinase complex Homo sapiens 36-53 20226165-4 2010 Celastrol (i) inhibits directly the IKKalpha and beta kinases, (ii) inactivates the Cdc37 and p23 proteins which are co-chaperones of HSP90, (iii) inhibits the function of proteasomes, and (iv) activates the HSF1 and subsequently triggers the heat shock response. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 84-89 20154087-2 2010 As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells. celastrol 171-180 caspase 3 Homo sapiens 160-169 20154087-2 2010 As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells. celastrol 171-180 TNF superfamily member 10 Homo sapiens 197-202 20154087-8 2010 We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL. celastrol 111-120 TNF superfamily member 10 Homo sapiens 189-194 20154087-2 2010 As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells. celastrol 171-180 TNF superfamily member 10 Homo sapiens 265-270 20226165-4 2010 Celastrol (i) inhibits directly the IKKalpha and beta kinases, (ii) inactivates the Cdc37 and p23 proteins which are co-chaperones of HSP90, (iii) inhibits the function of proteasomes, and (iv) activates the HSF1 and subsequently triggers the heat shock response. celastrol 0-9 prostaglandin E synthase 3 Homo sapiens 94-97 20226165-4 2010 Celastrol (i) inhibits directly the IKKalpha and beta kinases, (ii) inactivates the Cdc37 and p23 proteins which are co-chaperones of HSP90, (iii) inhibits the function of proteasomes, and (iv) activates the HSF1 and subsequently triggers the heat shock response. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 134-139 20154087-2 2010 As indicated by assays that measure plasma membrane integrity, phosphatidylserine exposure, mitochondrial activity, and activation of caspase-8, caspase-9, and caspase-3, celastrol potentiated the TRAIL-induced apoptosis in human breast cancer cells, and converted TRAIL-resistant cells to TRAIL-sensitive cells. celastrol 171-180 TNF superfamily member 10 Homo sapiens 265-270 20154087-4 2010 In addition, we found that celastrol induced the cell surface expression of both the TRAIL receptors DR4 and DR5. celastrol 27-36 TNF superfamily member 10 Homo sapiens 85-90 20154087-4 2010 In addition, we found that celastrol induced the cell surface expression of both the TRAIL receptors DR4 and DR5. celastrol 27-36 major histocompatibility complex, class II, DR beta 4 Homo sapiens 101-104 20154087-4 2010 In addition, we found that celastrol induced the cell surface expression of both the TRAIL receptors DR4 and DR5. celastrol 27-36 TNF receptor superfamily member 10b Homo sapiens 109-112 20154087-6 2010 Gene silencing of the death receptor abolished the effect of celastrol on TRAIL-induced apoptosis. celastrol 61-70 TNF superfamily member 10 Homo sapiens 74-79 20226165-4 2010 Celastrol (i) inhibits directly the IKKalpha and beta kinases, (ii) inactivates the Cdc37 and p23 proteins which are co-chaperones of HSP90, (iii) inhibits the function of proteasomes, and (iv) activates the HSF1 and subsequently triggers the heat shock response. celastrol 0-9 heat shock transcription factor 1 Homo sapiens 208-212 20154087-9 2010 Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CHOP pathway. celastrol 38-47 TNF superfamily member 10 Homo sapiens 88-93 20154087-7 2010 Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis. celastrol 251-260 DNA damage inducible transcript 3 Homo sapiens 164-168 20154087-7 2010 Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis. celastrol 251-260 DNA damage inducible transcript 3 Homo sapiens 201-205 20154087-9 2010 Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CHOP pathway. celastrol 38-47 DNA damage inducible transcript 3 Homo sapiens 219-223 19916747-2 2010 Moreover, the in vivo antitumor efficacy of TRAIL/APO-2L was dramatically increased by celastrol. celastrol 87-96 TNF superfamily member 10 Homo sapiens 44-49 20346213-0 2010 Effects of Celastrol on growth inhibition of U937 leukemia cells through the regulation of the Notch1/NF-kappaB signaling pathway in vitro. celastrol 11-20 notch receptor 1 Homo sapiens 95-101 20346213-0 2010 Effects of Celastrol on growth inhibition of U937 leukemia cells through the regulation of the Notch1/NF-kappaB signaling pathway in vitro. celastrol 11-20 nuclear factor kappa B subunit 1 Homo sapiens 102-111 20346213-13 2010 Overexpression of Notch1 was found in U937 cells, while Celastrol could downregulate it at both the protein and mRNA level in a dose-dependent manner, and expression of NF-kappaB decreased in nuclei and increased in the cytoplasm (P < 0.05). celastrol 56-65 notch receptor 1 Homo sapiens 18-24 20211007-5 2010 We therefore explored whether the known NFkappaB inhibitor celastrol could represent a suitable compound for decreasing Abeta production and accumulation in vivo. celastrol 59-68 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 40-48 20211007-5 2010 We therefore explored whether the known NFkappaB inhibitor celastrol could represent a suitable compound for decreasing Abeta production and accumulation in vivo. celastrol 59-68 amyloid beta (A4) precursor protein Mus musculus 120-125 20211007-6 2010 METHODS: The effect of celastrol on amyloid precursor protein (APP) processing, Abeta production and NFkappaB activation was investigated by western blotting and ELISAs using a cell line overexpressing APP. celastrol 23-32 amyloid beta (A4) precursor protein Mus musculus 36-61 20211007-8 2010 An acute treatment with celastrol was investigated by administering celastrol intraperitoneally at a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. celastrol 24-33 presenilin 1 Mus musculus 137-152 20211007-8 2010 An acute treatment with celastrol was investigated by administering celastrol intraperitoneally at a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. celastrol 68-77 presenilin 1 Mus musculus 137-152 20211007-9 2010 In addition, a chronic treatment (32 days) with celastrol was tested using a matrix-driven delivery pellet system implanted subcutaneously in 5 month-old Tg PS1/APPsw to ensure a continuous daily release of 2.5 mg/Kg of celastrol. celastrol 48-57 presenilin 1 Homo sapiens 157-160 20211007-10 2010 RESULTS: In vitro, celastrol dose dependently prevented NFkappaB activation and inhibited BACE-1 expression. celastrol 19-28 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 56-64 20211007-10 2010 RESULTS: In vitro, celastrol dose dependently prevented NFkappaB activation and inhibited BACE-1 expression. celastrol 19-28 beta-site APP cleaving enzyme 1 Mus musculus 90-96 20211007-13 2010 In addition, a reduction in Abeta plaque burden and microglial activation was observed in the brains of Tg PS1/APPsw following a chronic administration of celastrol. celastrol 155-164 amyloid beta (A4) precursor protein Mus musculus 28-33 20211007-13 2010 In addition, a reduction in Abeta plaque burden and microglial activation was observed in the brains of Tg PS1/APPsw following a chronic administration of celastrol. celastrol 155-164 presenilin 1 Homo sapiens 107-110 20211007-14 2010 CONCLUSIONS: Overall our data suggest that celastrol is a potent Abeta lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFkappaB dependent mechanism. celastrol 43-52 amyloid beta (A4) precursor protein Mus musculus 65-70 20211007-14 2010 CONCLUSIONS: Overall our data suggest that celastrol is a potent Abeta lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFkappaB dependent mechanism. celastrol 43-52 beta-site APP cleaving enzyme 1 Mus musculus 114-120 20211007-14 2010 CONCLUSIONS: Overall our data suggest that celastrol is a potent Abeta lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFkappaB dependent mechanism. celastrol 43-52 beta-site APP cleaving enzyme 1 Mus musculus 154-160 20211007-14 2010 CONCLUSIONS: Overall our data suggest that celastrol is a potent Abeta lowering compound that acts as an indirect BACE-1 inhibitor possibly by regulating BACE-1 expression level via an NFkappaB dependent mechanism. celastrol 43-52 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 185-193 20160026-0 2010 Celastrol suppresses angiogenesis-mediated tumor growth through inhibition of AKT/mammalian target of rapamycin pathway. celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 78-81 20160026-0 2010 Celastrol suppresses angiogenesis-mediated tumor growth through inhibition of AKT/mammalian target of rapamycin pathway. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 82-111 20160026-6 2010 Furthermore, Celastrol abrogated VEGF-induced sprouting of the vessels from aortic rings and inhibited vascular formation in the Matrigel plug assay in vivo. celastrol 13-22 vascular endothelial growth factor A Homo sapiens 33-37 20160026-8 2010 Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). celastrol 0-9 vascular endothelial growth factor A Homo sapiens 25-29 20160026-8 2010 Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). celastrol 0-9 AKT serine/threonine kinase 1 Homo sapiens 52-55 20160026-8 2010 Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 57-86 20160026-8 2010 Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 88-92 20160026-8 2010 Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K). celastrol 0-9 ribosomal protein S6 kinase B1 Homo sapiens 128-134 20160026-9 2010 Additionally, we found that Celastrol inhibited the proliferation of prostate cancer cells and induced apoptosis, and these effects correlated with the extent of inhibition of AKT/mTOR/P70S6K signaling. celastrol 28-37 AKT serine/threonine kinase 1 Homo sapiens 176-179 20160026-9 2010 Additionally, we found that Celastrol inhibited the proliferation of prostate cancer cells and induced apoptosis, and these effects correlated with the extent of inhibition of AKT/mTOR/P70S6K signaling. celastrol 28-37 mechanistic target of rapamycin kinase Homo sapiens 180-184 20160026-9 2010 Additionally, we found that Celastrol inhibited the proliferation of prostate cancer cells and induced apoptosis, and these effects correlated with the extent of inhibition of AKT/mTOR/P70S6K signaling. celastrol 28-37 ribosomal protein S6 kinase B1 Homo sapiens 185-191 20160026-10 2010 Taken together, our results suggest that Celastrol targets the AKT/mTOR/P70S6K pathway, which leads to suppression of tumor growth and angiogenesis. celastrol 41-50 AKT serine/threonine kinase 1 Homo sapiens 63-66 20160026-10 2010 Taken together, our results suggest that Celastrol targets the AKT/mTOR/P70S6K pathway, which leads to suppression of tumor growth and angiogenesis. celastrol 41-50 mechanistic target of rapamycin kinase Homo sapiens 67-71 20160026-10 2010 Taken together, our results suggest that Celastrol targets the AKT/mTOR/P70S6K pathway, which leads to suppression of tumor growth and angiogenesis. celastrol 41-50 ribosomal protein S6 kinase B1 Homo sapiens 72-78 20007406-2 2010 Celastrol, isolated from a Chinese medicinal herb, is a novel heat shock protein 90 (Hsp90) inhibitor with potent anticancer activity against glioma in vitro and in vivo. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 62-83 20007406-2 2010 Celastrol, isolated from a Chinese medicinal herb, is a novel heat shock protein 90 (Hsp90) inhibitor with potent anticancer activity against glioma in vitro and in vivo. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 85-90 20007406-3 2010 In search of correlations between growth-inhibitory potency of celastrol in NCI-60 cell lines and microarray expression profiles of most known transporters, we found that expression of SLC7A11, the gene encoding the light chain subunit of x(c)(-), showed a strong negative correlation with celastrol activity. celastrol 63-72 solute carrier family 7 member 11 Homo sapiens 185-192 20007406-3 2010 In search of correlations between growth-inhibitory potency of celastrol in NCI-60 cell lines and microarray expression profiles of most known transporters, we found that expression of SLC7A11, the gene encoding the light chain subunit of x(c)(-), showed a strong negative correlation with celastrol activity. celastrol 290-299 solute carrier family 7 member 11 Homo sapiens 185-192 20007406-5 2010 In celastrol-resistant glioma cells that highly expressed SLC7A11, sensitivity to celastrol was consistently increased via treatment with x(c)(-) inhibitors, including glutamate, (S)-4-carboxyphenylglycine, sulfasalazine, and SLC7A11 small interfering RNA. celastrol 3-12 solute carrier family 7 member 11 Homo sapiens 58-65 20007406-5 2010 In celastrol-resistant glioma cells that highly expressed SLC7A11, sensitivity to celastrol was consistently increased via treatment with x(c)(-) inhibitors, including glutamate, (S)-4-carboxyphenylglycine, sulfasalazine, and SLC7A11 small interfering RNA. celastrol 82-91 solute carrier family 7 member 11 Homo sapiens 58-65 20007406-5 2010 In celastrol-resistant glioma cells that highly expressed SLC7A11, sensitivity to celastrol was consistently increased via treatment with x(c)(-) inhibitors, including glutamate, (S)-4-carboxyphenylglycine, sulfasalazine, and SLC7A11 small interfering RNA. celastrol 82-91 solute carrier family 7 member 11 Homo sapiens 226-233 20007406-8 2010 Combined treatment of glioma cells with sulfasalazine and celastrol led to chemosensitization, as suggested by increased celastrol-induced cell cycle arrest, apoptosis, and down-regulation of the Hsp90 client protein, epidermal growth factor receptor. celastrol 58-67 heat shock protein 90 alpha family class A member 1 Homo sapiens 196-201 20007406-8 2010 Combined treatment of glioma cells with sulfasalazine and celastrol led to chemosensitization, as suggested by increased celastrol-induced cell cycle arrest, apoptosis, and down-regulation of the Hsp90 client protein, epidermal growth factor receptor. celastrol 58-67 epidermal growth factor receptor Homo sapiens 218-250 20007406-8 2010 Combined treatment of glioma cells with sulfasalazine and celastrol led to chemosensitization, as suggested by increased celastrol-induced cell cycle arrest, apoptosis, and down-regulation of the Hsp90 client protein, epidermal growth factor receptor. celastrol 121-130 heat shock protein 90 alpha family class A member 1 Homo sapiens 196-201 19996313-0 2010 Celastrol inhibits Hsp90 chaperoning of steroid receptors by inducing fibrillization of the Co-chaperone p23. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 19-24 19996313-0 2010 Celastrol inhibits Hsp90 chaperoning of steroid receptors by inducing fibrillization of the Co-chaperone p23. celastrol 0-9 prostaglandin E synthase 3 Homo sapiens 105-108 19996313-3 2010 Here, we show that the small molecule celastrol inhibits the Hsp90 chaperoning machinery by inactivating the co-chaperone p23, resulting in a more selective destabilization of steroid receptors compared with kinase clients. celastrol 38-47 heat shock protein 90 alpha family class A member 1 Homo sapiens 61-66 19996313-3 2010 Here, we show that the small molecule celastrol inhibits the Hsp90 chaperoning machinery by inactivating the co-chaperone p23, resulting in a more selective destabilization of steroid receptors compared with kinase clients. celastrol 38-47 prostaglandin E synthase 3 Homo sapiens 122-125 19996313-4 2010 Our in vitro and in vivo results demonstrate that celastrol disrupts p23 function by altering its three-dimensional structure, leading to rapid formation of amyloid-like fibrils. celastrol 50-59 prostaglandin E synthase 3 Homo sapiens 69-72 19916747-2 2010 Moreover, the in vivo antitumor efficacy of TRAIL/APO-2L was dramatically increased by celastrol. celastrol 87-96 TNF superfamily member 10 Homo sapiens 50-56 19916747-4 2010 Taken together, our data firstly demonstrate the synergistic anticancer capabilities achieved by combining TRAIL/APO-2L and celastrol, and moreover, open new opportunities to enhance the effectiveness of future treatment regimens using TRAIL/APO-2L. celastrol 124-133 TNF superfamily member 10 Homo sapiens 236-248 19858214-7 2009 Celastrol inhibits Hsp90 ATPase activity without blocking ATP binding. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 19-24 19858214-8 2009 Proteolytic fingerprinting indicates celastrol binds to Hsp90 C-terminal domain to protect it from trypsin digestion. celastrol 37-46 heat shock protein 90 alpha family class A member 1 Homo sapiens 56-61 19858214-0 2009 Characterization of celastrol to inhibit hsp90 and cdc37 interaction. celastrol 20-29 heat shock protein 90 alpha family class A member 1 Homo sapiens 41-46 19858214-9 2009 These data suggest that celastrol may represent a new class of Hsp90 inhibitor by modifying Hsp90 C terminus to allosterically regulate its chaperone activity and disrupt Hsp90-Cdc37 complex. celastrol 24-33 heat shock protein 90 alpha family class A member 1 Homo sapiens 63-68 19858214-0 2009 Characterization of celastrol to inhibit hsp90 and cdc37 interaction. celastrol 20-29 cell division cycle 37, HSP90 cochaperone Homo sapiens 51-56 19858214-9 2009 These data suggest that celastrol may represent a new class of Hsp90 inhibitor by modifying Hsp90 C terminus to allosterically regulate its chaperone activity and disrupt Hsp90-Cdc37 complex. celastrol 24-33 heat shock protein 90 alpha family class A member 1 Homo sapiens 92-97 19858214-6 2009 Celastrol disrupts Hsp90-Cdc37 complex formation, whereas the classical Hsp90 inhibitors (e.g. geldanamycin) have no effect. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 19-24 19858214-6 2009 Celastrol disrupts Hsp90-Cdc37 complex formation, whereas the classical Hsp90 inhibitors (e.g. geldanamycin) have no effect. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 25-30 19858214-9 2009 These data suggest that celastrol may represent a new class of Hsp90 inhibitor by modifying Hsp90 C terminus to allosterically regulate its chaperone activity and disrupt Hsp90-Cdc37 complex. celastrol 24-33 heat shock protein 90 alpha family class A member 1 Homo sapiens 92-97 19858214-9 2009 These data suggest that celastrol may represent a new class of Hsp90 inhibitor by modifying Hsp90 C terminus to allosterically regulate its chaperone activity and disrupt Hsp90-Cdc37 complex. celastrol 24-33 cell division cycle 37, HSP90 cochaperone Homo sapiens 177-182 19934274-8 2009 CEL treatment increased the levels of ubiquitinated proteins, reduced the levels of tumor necrosis factor-alpha-induced IkappaB phosphorylation, and blocked NF-kappaB translocation to the nucleus. celastrol 0-3 tumor necrosis factor Homo sapiens 84-111 19934274-8 2009 CEL treatment increased the levels of ubiquitinated proteins, reduced the levels of tumor necrosis factor-alpha-induced IkappaB phosphorylation, and blocked NF-kappaB translocation to the nucleus. celastrol 0-3 nuclear factor kappa B subunit 1 Homo sapiens 157-166 19934274-9 2009 Inhibition of NF-kappaB with small interfering RNA mimicked the ability of CEL to sensitize melanoma cells to TMZ, suggesting that inhibition of NF-kappaB may play a role in TMZ/CEL-induced cytotoxicity. celastrol 75-78 nuclear factor kappa B subunit 1 Homo sapiens 14-23 19934274-9 2009 Inhibition of NF-kappaB with small interfering RNA mimicked the ability of CEL to sensitize melanoma cells to TMZ, suggesting that inhibition of NF-kappaB may play a role in TMZ/CEL-induced cytotoxicity. celastrol 75-78 nuclear factor kappa B subunit 1 Homo sapiens 145-154 19671767-5 2009 Celastrol, BMS-345541, and parthenolide abolished IL1beta and tumor necrosis factor alpha-induced IkappaB phosphorylation and prevented nuclear translocation of NF-kappaB and DNA binding. celastrol 0-9 interleukin 1 beta Rattus norvegicus 50-57 19778460-0 2009 The NF-kappa B inhibitor, celastrol, could enhance the anti-cancer effect of gambogic acid on oral squamous cell carcinoma. celastrol 26-35 nuclear factor kappa B subunit 1 Homo sapiens 4-14 19778460-3 2009 In this study, the effects and mechanisms of GA and the NF-kappa B inhibitor celastrol on oral cancer cells were investigated. celastrol 77-86 nuclear factor kappa B subunit 1 Homo sapiens 56-66 19778460-10 2009 The minimal cytotoxic dose of celastrol was able to effectively suppress the GA-induced NF-kappa B pathway activation. celastrol 30-39 nuclear factor kappa B subunit 1 Homo sapiens 88-98 19723328-11 2009 We show that celastrol and minocycline, both having antioxidant and anti-inflammatory properties, confer potent dopaminergic neuroprotection in Drosophila DJ-1A model, while coQ10 shows no protective effect. celastrol 13-22 DJ-1alpha Drosophila melanogaster 155-160 19661812-4 2009 In in vitro experiments with human platelets, celastrol inhibits adenosine-5-diphosphate (ADP)-induced expression of the platelet activation marker P-selectin and glycoprotein IIb/IIIa activation with 50% inhibition values of 1.62 and 1.86 microM, respectively. celastrol 46-55 selectin P Homo sapiens 148-158 19661812-5 2009 Celastrol also inhibits thrombin-stimulated and phorbol 12-myristate 13-acetate-stimulated P-selectin expression on platelets. celastrol 0-9 selectin P Homo sapiens 91-101 19671767-6 2009 Celastrol and parthenolide but not BMS-345541 prevented the activation of both IKKalpha and IKKbeta, and celastrol inhibited IKKalpha/beta activation by preventing the phosphorylation of TAK1, a key receptor-associated factor upstream of IKK. celastrol 105-114 component of inhibitor of nuclear factor kappa B kinase complex Rattus norvegicus 125-133 19671767-6 2009 Celastrol and parthenolide but not BMS-345541 prevented the activation of both IKKalpha and IKKbeta, and celastrol inhibited IKKalpha/beta activation by preventing the phosphorylation of TAK1, a key receptor-associated factor upstream of IKK. celastrol 105-114 mitogen activated protein kinase kinase kinase 7 Rattus norvegicus 187-241 19671767-7 2009 Celastrol and parthenolide markedly reduced the mRNA expression of matrix metalloproteinase 9 and urinary plasminogen activator, and inhibited W256 migration. celastrol 0-9 matrix metallopeptidase 9 Rattus norvegicus 67-93 19549173-5 2009 RESULTS: Our in vitro experiments showed that celastrol suppressed not only LPS-stimulated generation of nitric oxide and prostaglandin E(2), but also expression of inducible nitric oxide synthase and cyclooxygenase-2 in RAW264.7 cells. celastrol 46-55 prostaglandin-endoperoxide synthase 2 Mus musculus 201-217 19549173-6 2009 Similarly, celastrol inhibited LPS-induced production of inflammatory cytokines, including tumour necrosis factor-alpha and interleukin-6. celastrol 11-20 interleukin 6 Mus musculus 124-137 19549173-7 2009 In an animal model, celastrol protected mice from TPA-induced ear oedema, possibly by inhibiting MPO activity and production of inflammatory cytokines. celastrol 20-29 myeloperoxidase Mus musculus 97-100 19671767-5 2009 Celastrol, BMS-345541, and parthenolide abolished IL1beta and tumor necrosis factor alpha-induced IkappaB phosphorylation and prevented nuclear translocation of NF-kappaB and DNA binding. celastrol 0-9 tumor necrosis factor Rattus norvegicus 62-89 19671767-6 2009 Celastrol and parthenolide but not BMS-345541 prevented the activation of both IKKalpha and IKKbeta, and celastrol inhibited IKKalpha/beta activation by preventing the phosphorylation of TAK1, a key receptor-associated factor upstream of IKK. celastrol 0-9 component of inhibitor of nuclear factor kappa B kinase complex Rattus norvegicus 79-87 19671767-6 2009 Celastrol and parthenolide but not BMS-345541 prevented the activation of both IKKalpha and IKKbeta, and celastrol inhibited IKKalpha/beta activation by preventing the phosphorylation of TAK1, a key receptor-associated factor upstream of IKK. celastrol 0-9 inhibitor of nuclear factor kappa B kinase subunit beta Rattus norvegicus 92-99 19508391-7 2009 LPS + IFNgamma stimulated phosphorylation of ERK, JNK and Jak2, and degradation of IkappaB, but only Jak2 phosphorylation was sensitive to tripterine (50-200 nM). celastrol 139-149 Janus kinase 2 Mus musculus 101-105 19719969-12 2009 Celastrol at each different dose level lowered the density of MVD significantly in tumor bearing nude mice compared to the control group. celastrol 0-9 mevalonate (diphospho) decarboxylase Mus musculus 62-65 19719969-13 2009 Immunohistochemistry experiments further revealed that celastrol also decreased the level of VEGFR-1 and VEGFR-2 expression, but not the level of VEGF expression. celastrol 55-64 fms related receptor tyrosine kinase 1 Homo sapiens 93-100 19719969-13 2009 Immunohistochemistry experiments further revealed that celastrol also decreased the level of VEGFR-1 and VEGFR-2 expression, but not the level of VEGF expression. celastrol 55-64 kinase insert domain receptor Homo sapiens 105-112 19719969-13 2009 Immunohistochemistry experiments further revealed that celastrol also decreased the level of VEGFR-1 and VEGFR-2 expression, but not the level of VEGF expression. celastrol 55-64 vascular endothelial growth factor A Homo sapiens 93-97 19322522-5 2009 Celastrol-resistant B16F10 melanoma cells had a higher expression level of c-FLIP(L) and Snail as compared with a sensitive cell line. celastrol 0-9 CASP8 and FADD-like apoptosis regulator Mus musculus 75-81 19322522-5 2009 Celastrol-resistant B16F10 melanoma cells had a higher expression level of c-FLIP(L) and Snail as compared with a sensitive cell line. celastrol 0-9 snail family zinc finger 1 Mus musculus 89-94 19508391-5 2009 These effects of LPS + IFNgamma were diminished by tripterine (50-200 nM). celastrol 51-61 interferon gamma Mus musculus 23-31 19508391-9 2009 CONCLUSION AND IMPLICATIONS: Our results indicate that, by preventing Jak2-dependent induction of iNOS and Nox1, tripterine inhibits peroxynitrite precursor synthesis, attenuates the increased activity of PP2A and consequently protects endothelial barrier function. celastrol 113-123 Janus kinase 2 Mus musculus 70-74 19508391-9 2009 CONCLUSION AND IMPLICATIONS: Our results indicate that, by preventing Jak2-dependent induction of iNOS and Nox1, tripterine inhibits peroxynitrite precursor synthesis, attenuates the increased activity of PP2A and consequently protects endothelial barrier function. celastrol 113-123 nitric oxide synthase 2, inducible Mus musculus 98-102 19508391-9 2009 CONCLUSION AND IMPLICATIONS: Our results indicate that, by preventing Jak2-dependent induction of iNOS and Nox1, tripterine inhibits peroxynitrite precursor synthesis, attenuates the increased activity of PP2A and consequently protects endothelial barrier function. celastrol 113-123 NADPH oxidase 1 Mus musculus 107-111 19508391-9 2009 CONCLUSION AND IMPLICATIONS: Our results indicate that, by preventing Jak2-dependent induction of iNOS and Nox1, tripterine inhibits peroxynitrite precursor synthesis, attenuates the increased activity of PP2A and consequently protects endothelial barrier function. celastrol 113-123 protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform Mus musculus 205-209 19356729-0 2009 Celastrol binds to ERK and inhibits FcepsilonRI signaling to exert an anti-allergic effect. celastrol 0-9 Eph receptor B1 Rattus norvegicus 19-22 19356729-2 2009 Celastrol decreased the secretion of beta-hexosaminidase, decreased the release of histamine, decreased the expression of Th2 cytokines and decreased calcium influx and cell adhesion in antigen-stimulated RBL2H3 cells. celastrol 0-9 O-GlcNAcase Rattus norvegicus 37-56 19356734-5 2009 Celastrol reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid and in peribronchial areas, and decreased the airway hyperresponsiveness, mRNA and protein expression levels for inflammatory cytokines such as interleukin (IL)-4, IL-13, TNF-alpha and IFN-gamma, and for MMPs and TIMPs, MAP kinases and NF-kappaB activities in the bronchoalveolar lavage cells and in the lung tissues increased in ovalbumin-induced allergic asthma in mice. celastrol 0-9 tumor necrosis factor Mus musculus 264-273 19356734-5 2009 Celastrol reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid and in peribronchial areas, and decreased the airway hyperresponsiveness, mRNA and protein expression levels for inflammatory cytokines such as interleukin (IL)-4, IL-13, TNF-alpha and IFN-gamma, and for MMPs and TIMPs, MAP kinases and NF-kappaB activities in the bronchoalveolar lavage cells and in the lung tissues increased in ovalbumin-induced allergic asthma in mice. celastrol 0-9 interferon gamma Mus musculus 278-287 19356729-2 2009 Celastrol decreased the secretion of beta-hexosaminidase, decreased the release of histamine, decreased the expression of Th2 cytokines and decreased calcium influx and cell adhesion in antigen-stimulated RBL2H3 cells. celastrol 0-9 RB transcriptional corepressor like 2 Rattus norvegicus 205-209 19356734-5 2009 Celastrol reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid and in peribronchial areas, and decreased the airway hyperresponsiveness, mRNA and protein expression levels for inflammatory cytokines such as interleukin (IL)-4, IL-13, TNF-alpha and IFN-gamma, and for MMPs and TIMPs, MAP kinases and NF-kappaB activities in the bronchoalveolar lavage cells and in the lung tissues increased in ovalbumin-induced allergic asthma in mice. celastrol 0-9 matrix metallopeptidase 2 Mus musculus 297-301 19356729-3 2009 Exposure to celastrol decreased the phosphorylation of extracellular regulated kinase (ERK) and the ERK kinase activity was decreased in RBL2H3 cells. celastrol 12-21 Eph receptor B1 Rattus norvegicus 55-85 19356734-5 2009 Celastrol reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid and in peribronchial areas, and decreased the airway hyperresponsiveness, mRNA and protein expression levels for inflammatory cytokines such as interleukin (IL)-4, IL-13, TNF-alpha and IFN-gamma, and for MMPs and TIMPs, MAP kinases and NF-kappaB activities in the bronchoalveolar lavage cells and in the lung tissues increased in ovalbumin-induced allergic asthma in mice. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 329-338 19356734-5 2009 Celastrol reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid and in peribronchial areas, and decreased the airway hyperresponsiveness, mRNA and protein expression levels for inflammatory cytokines such as interleukin (IL)-4, IL-13, TNF-alpha and IFN-gamma, and for MMPs and TIMPs, MAP kinases and NF-kappaB activities in the bronchoalveolar lavage cells and in the lung tissues increased in ovalbumin-induced allergic asthma in mice. celastrol 0-9 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 423-432 19356729-3 2009 Exposure to celastrol decreased the phosphorylation of extracellular regulated kinase (ERK) and the ERK kinase activity was decreased in RBL2H3 cells. celastrol 12-21 Eph receptor B1 Rattus norvegicus 87-90 19356734-6 2009 Our data suggest that oral administration of celastrol suppresses ovalbumin-induced airway inflammation, hyperresponsiveness, and tissue remodeling by regulating the imbalance of MMP-2/-9 and TIMP-1/-2 by inflammatory cytokines via MAP kinases/NF-kappaB in inflammatory cells. celastrol 45-54 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 66-75 19356729-3 2009 Exposure to celastrol decreased the phosphorylation of extracellular regulated kinase (ERK) and the ERK kinase activity was decreased in RBL2H3 cells. celastrol 12-21 Eph receptor B1 Rattus norvegicus 100-103 19356734-6 2009 Our data suggest that oral administration of celastrol suppresses ovalbumin-induced airway inflammation, hyperresponsiveness, and tissue remodeling by regulating the imbalance of MMP-2/-9 and TIMP-1/-2 by inflammatory cytokines via MAP kinases/NF-kappaB in inflammatory cells. celastrol 45-54 matrix metallopeptidase 2 Mus musculus 179-187 19356734-6 2009 Our data suggest that oral administration of celastrol suppresses ovalbumin-induced airway inflammation, hyperresponsiveness, and tissue remodeling by regulating the imbalance of MMP-2/-9 and TIMP-1/-2 by inflammatory cytokines via MAP kinases/NF-kappaB in inflammatory cells. celastrol 45-54 tissue inhibitor of metalloproteinase 1 Mus musculus 192-198 19356734-6 2009 Our data suggest that oral administration of celastrol suppresses ovalbumin-induced airway inflammation, hyperresponsiveness, and tissue remodeling by regulating the imbalance of MMP-2/-9 and TIMP-1/-2 by inflammatory cytokines via MAP kinases/NF-kappaB in inflammatory cells. celastrol 45-54 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 244-253 19356729-4 2009 A molecular dynamics simulation showed binding of celastrol to a large pocket in ERK2, which serves as the ATP-binding site. celastrol 50-59 mitogen activated protein kinase 1 Rattus norvegicus 81-85 19356729-5 2009 Exposure to celastrol inhibited the interaction between immunoglobulin Fc epsilon receptor I (FcepsilonRIgamma) and ERK and inhibited interaction between FcepsilonRIgamma and protein kinase C delta (PKCdelta). celastrol 12-21 Eph receptor B1 Rattus norvegicus 56-119 19356729-8 2009 Celastrol regulated the expression of epithelial-mesenchymal transition (EMT)-related proteins through inhibition of PKCalpha, PKCdelta, and Rac1 in antigen-stimulated RBL2H3 cells. celastrol 0-9 protein kinase C, alpha Rattus norvegicus 117-125 19356729-8 2009 Celastrol regulated the expression of epithelial-mesenchymal transition (EMT)-related proteins through inhibition of PKCalpha, PKCdelta, and Rac1 in antigen-stimulated RBL2H3 cells. celastrol 0-9 Rac family small GTPase 1 Rattus norvegicus 141-145 19356729-8 2009 Celastrol regulated the expression of epithelial-mesenchymal transition (EMT)-related proteins through inhibition of PKCalpha, PKCdelta, and Rac1 in antigen-stimulated RBL2H3 cells. celastrol 0-9 RB transcriptional corepressor like 2 Rattus norvegicus 168-172 19356729-10 2009 Celastrol exerted a negative effect on FcepsilonRIbeta signaling by inhibiting the interaction between heat shock protein 90 (hsp90) and proteins, such as, FcepsilonRIbeta, Akt and PKCalpha. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 103-124 19356729-10 2009 Celastrol exerted a negative effect on FcepsilonRIbeta signaling by inhibiting the interaction between heat shock protein 90 (hsp90) and proteins, such as, FcepsilonRIbeta, Akt and PKCalpha. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 126-131 19356729-10 2009 Celastrol exerted a negative effect on FcepsilonRIbeta signaling by inhibiting the interaction between heat shock protein 90 (hsp90) and proteins, such as, FcepsilonRIbeta, Akt and PKCalpha. celastrol 0-9 AKT serine/threonine kinase 1 Rattus norvegicus 173-176 19356729-10 2009 Celastrol exerted a negative effect on FcepsilonRIbeta signaling by inhibiting the interaction between heat shock protein 90 (hsp90) and proteins, such as, FcepsilonRIbeta, Akt and PKCalpha. celastrol 0-9 protein kinase C, alpha Rattus norvegicus 181-189 19356729-11 2009 Celastrol exerted a negative effect on in vivo atopic dermatitis induced by 2, 4-dinitrofluorobenzene (DNFB), which requires ERK. celastrol 0-9 Eph receptor B1 Rattus norvegicus 125-128 19356729-13 2009 In summary, celastrol binds to ERK and inhibits FcepsilonRI signaling to exert an anti-inflammatory effect. celastrol 12-21 Eph receptor B1 Rattus norvegicus 31-34 19183864-4 2009 Although both arimoclomol and celastrol induced the expression of Hsp70, their effects on primary motoneurons in culture were significantly different. celastrol 30-39 heat shock protein 1B Mus musculus 66-71 19585625-0 2009 Molecular mechanism of inhibition of the human protein complex Hsp90-Cdc37, a kinome chaperone-cochaperone, by triterpene celastrol. celastrol 122-131 heat shock protein 90 alpha family class A member 1 Homo sapiens 63-68 19585625-0 2009 Molecular mechanism of inhibition of the human protein complex Hsp90-Cdc37, a kinome chaperone-cochaperone, by triterpene celastrol. celastrol 122-131 cell division cycle 37, HSP90 cochaperone Homo sapiens 69-74 19183864-6 2009 Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. celastrol 18-27 heat shock protein 1B Mus musculus 49-54 19183864-6 2009 Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. celastrol 18-27 caspase 3 Mus musculus 69-78 19183864-6 2009 Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. celastrol 93-102 heat shock protein 1B Mus musculus 49-54 19183864-6 2009 Immunostaining of celastrol-treated cultures for hsp70 and activated caspase-3 revealed that celastrol treatment activates both the heat shock response and the apoptotic cell death cascade. celastrol 93-102 caspase 3 Mus musculus 69-78 18726991-3 2008 We have previously reported that apoptosis induced by medicinal proteasome-inhibitory compound celastrol is associated with a decrease in AR protein levels. celastrol 95-104 androgen receptor Homo sapiens 138-140 18726991-4 2008 However celastrol-stimulated events contributing to this AR decrease have not been elucidated. celastrol 8-17 androgen receptor Homo sapiens 57-59 18726991-8 2008 Interestingly, proteasome inhibitor celastrol- and chemotherapeutic drug VP-16-stimulated AR breakdown was attenuated by calpain inhibitors calpastatin and N-acetyl-L-leucyl-L-leucyl-L-methioninal. celastrol 36-45 androgen receptor Homo sapiens 90-92 18726991-9 2008 Furthermore, AR proteolytic activity pulled down by calmodulin-agarose beads from celastrol-treated PC-3 cells showed immunoreactivity to a calpain antibody. celastrol 82-91 androgen receptor Homo sapiens 13-15 18577440-7 2008 The effects of tripterine were associated with decreased interleukin-1beta (IL-1beta) mRNA expression in ankle joint synovial membrane and tumor necrosis factor-alpha (TNF-alpha) mRNA expression in homogenized paws from adjuvant-induced arthritic rats. celastrol 15-25 interleukin 1 beta Rattus norvegicus 57-74 19138996-5 2008 Inhibitors of HSP90 [17-allylamino-17-demethoxygeldanamycin (17-AAG); celastrol] suppressed these inductive effects of PAHs. celastrol 70-79 heat shock protein 90 alpha family class A member 1 Homo sapiens 14-19 19138996-6 2008 Treatment with 17-AAG and celastrol also caused a rapid and marked decrease in amounts of AhR protein without modulating levels of HSP90. celastrol 26-35 aryl hydrocarbon receptor Homo sapiens 90-93 19138996-6 2008 Treatment with 17-AAG and celastrol also caused a rapid and marked decrease in amounts of AhR protein without modulating levels of HSP90. celastrol 26-35 heat shock protein 90 alpha family class A member 1 Homo sapiens 131-136 19138996-7 2008 The formation of B(a)P-induced DNA adducts in MSK-Leuk1 cells was inhibited by 17-AAG, celastrol, and alpha-naphthoflavone, a known AhR antagonist. celastrol 87-96 aryl hydrocarbon receptor Homo sapiens 132-135 19138996-8 2008 The reduction in B(a)P-induced DNA adducts was due, at least in part, to reduced metabolic activation of B(a)P. Collectively, these results suggest that 17-AAG and celastrol, inhibitors of HSP90, suppress the activation of AhR-dependent gene expression, leading, in turn, to reduced formation of B(a)P-induced DNA adducts. celastrol 164-173 heat shock protein 90 alpha family class A member 1 Homo sapiens 189-194 19138996-8 2008 The reduction in B(a)P-induced DNA adducts was due, at least in part, to reduced metabolic activation of B(a)P. Collectively, these results suggest that 17-AAG and celastrol, inhibitors of HSP90, suppress the activation of AhR-dependent gene expression, leading, in turn, to reduced formation of B(a)P-induced DNA adducts. celastrol 164-173 aryl hydrocarbon receptor Homo sapiens 223-226 18577440-7 2008 The effects of tripterine were associated with decreased interleukin-1beta (IL-1beta) mRNA expression in ankle joint synovial membrane and tumor necrosis factor-alpha (TNF-alpha) mRNA expression in homogenized paws from adjuvant-induced arthritic rats. celastrol 15-25 interleukin 1 beta Rattus norvegicus 76-84 18577440-7 2008 The effects of tripterine were associated with decreased interleukin-1beta (IL-1beta) mRNA expression in ankle joint synovial membrane and tumor necrosis factor-alpha (TNF-alpha) mRNA expression in homogenized paws from adjuvant-induced arthritic rats. celastrol 15-25 tumor necrosis factor Rattus norvegicus 139-166 18577440-7 2008 The effects of tripterine were associated with decreased interleukin-1beta (IL-1beta) mRNA expression in ankle joint synovial membrane and tumor necrosis factor-alpha (TNF-alpha) mRNA expression in homogenized paws from adjuvant-induced arthritic rats. celastrol 15-25 tumor necrosis factor Rattus norvegicus 168-177 17943263-2 2007 In this paper, we show that celastrol, a compound recently shown to up-regulate hsp gene expression, significantly decreases killing of cells expressing mutant polyglutamine protein. celastrol 28-37 heat shock protein 90 beta family member 2, pseudogene Homo sapiens 80-83 18202019-4 2008 Here, we reported that celastrol disrupted Hsp90-Cdc37 interaction in the superchaperone complex to exhibit antitumor activity in vitro and in vivo. celastrol 23-32 heat shock protein 86, pseudogene 1 Mus musculus 43-48 18202019-4 2008 Here, we reported that celastrol disrupted Hsp90-Cdc37 interaction in the superchaperone complex to exhibit antitumor activity in vitro and in vivo. celastrol 23-32 cell division cycle 37 Mus musculus 49-54 18202019-5 2008 Molecular docking and molecular dynamic simulations showed that celastrol blocked the critical interaction of Glu33 (Hsp90) and Arg167 (Cdc37). celastrol 64-73 heat shock protein 86, pseudogene 1 Mus musculus 117-122 18202019-5 2008 Molecular docking and molecular dynamic simulations showed that celastrol blocked the critical interaction of Glu33 (Hsp90) and Arg167 (Cdc37). celastrol 64-73 cell division cycle 37 Mus musculus 136-141 18202019-6 2008 Immunoprecipitation confirmed that celastrol (10 micromol/L) disrupted the Hsp90-Cdc37 interaction in the pancreatic cancer cell line Panc-1. celastrol 35-44 heat shock protein 86, pseudogene 1 Mus musculus 75-80 18202019-6 2008 Immunoprecipitation confirmed that celastrol (10 micromol/L) disrupted the Hsp90-Cdc37 interaction in the pancreatic cancer cell line Panc-1. celastrol 35-44 cell division cycle 37 Mus musculus 81-86 18202019-6 2008 Immunoprecipitation confirmed that celastrol (10 micromol/L) disrupted the Hsp90-Cdc37 interaction in the pancreatic cancer cell line Panc-1. celastrol 35-44 pancreas protein 1 Mus musculus 134-140 18202019-8 2008 However, celastrol (1-5 micromol/L) induced Hsp90 client protein degradation (Cdk4 and Akt) by 70% to 80% and increased Hsp70 expression by 12-fold. celastrol 9-18 heat shock protein 86, pseudogene 1 Mus musculus 44-49 18202019-8 2008 However, celastrol (1-5 micromol/L) induced Hsp90 client protein degradation (Cdk4 and Akt) by 70% to 80% and increased Hsp70 expression by 12-fold. celastrol 9-18 cyclin-dependent kinase 4 Mus musculus 78-82 18202019-8 2008 However, celastrol (1-5 micromol/L) induced Hsp90 client protein degradation (Cdk4 and Akt) by 70% to 80% and increased Hsp70 expression by 12-fold. celastrol 9-18 thymoma viral proto-oncogene 1 Mus musculus 87-90 18202019-8 2008 However, celastrol (1-5 micromol/L) induced Hsp90 client protein degradation (Cdk4 and Akt) by 70% to 80% and increased Hsp70 expression by 12-fold. celastrol 9-18 heat shock protein 1B Mus musculus 120-125 18202019-9 2008 Celastrol induced apoptosis in vitro and significantly inhibited tumor growth in Panc-1 xenografts. celastrol 0-9 pancreas protein 1 Mus musculus 81-87 18202019-10 2008 Moreover, celastrol (3 mg/kg) effectively suppressed tumor metastasis by more than 80% in RIP1-Tag2 transgenic mouse model with pancreatic islet cell carcinogenesis. celastrol 10-19 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 90-94 18202019-11 2008 The data suggest that celastrol is a novel Hsp90 inhibitor to disrupt Hsp90-Cdc37 interaction against pancreatic cancer cells. celastrol 22-31 heat shock protein 86, pseudogene 1 Mus musculus 43-48 18202019-11 2008 The data suggest that celastrol is a novel Hsp90 inhibitor to disrupt Hsp90-Cdc37 interaction against pancreatic cancer cells. celastrol 22-31 heat shock protein 86, pseudogene 1 Mus musculus 70-75 18202019-11 2008 The data suggest that celastrol is a novel Hsp90 inhibitor to disrupt Hsp90-Cdc37 interaction against pancreatic cancer cells. celastrol 22-31 cell division cycle 37 Mus musculus 76-81 18343027-4 2008 Interestingly, while celastrol had no effect on either the expression of VEGF or its mRNA levels, celastrol treatment lowered the expression levels of its receptors (VEGFR-1 and VEGFR-2) and their mRNA levels. celastrol 98-107 FMS-like tyrosine kinase 1 Mus musculus 166-173 18343027-4 2008 Interestingly, while celastrol had no effect on either the expression of VEGF or its mRNA levels, celastrol treatment lowered the expression levels of its receptors (VEGFR-1 and VEGFR-2) and their mRNA levels. celastrol 98-107 kinase insert domain protein receptor Mus musculus 178-185 18343027-5 2008 These findings suggest that celastrol have potential to be used as an antiangiogenesis drug through its role in suppressing VEGF receptors expression that might consequently reduce the signal transduction between VEGF and VEGFR. celastrol 28-37 vascular endothelial growth factor A Mus musculus 124-128 18343027-5 2008 These findings suggest that celastrol have potential to be used as an antiangiogenesis drug through its role in suppressing VEGF receptors expression that might consequently reduce the signal transduction between VEGF and VEGFR. celastrol 28-37 vascular endothelial growth factor A Mus musculus 213-217 18199679-3 2008 The quinone methide triterpene celastrol, derived from a traditional Chinese medicinal herb, has numerous pharmacological properties, and it is a potent activator of the mammalian heat shock transcription factor HSF1. celastrol 31-40 heat shock transcription factor 1 Homo sapiens 212-216 18199679-5 2008 We show here that celastrol activates Hsf1 in Saccharomyces cerevisiae at a similar effective concentration seen in mammalian cells. celastrol 18-27 stress-responsive transcription factor HSF1 Saccharomyces cerevisiae S288C 38-42 18199679-7 2008 Celastrol activated the yeast Yap1 oxidant defense transcription factor via the carboxy-terminal redox center that responds to electrophilic compounds. celastrol 0-9 DNA-binding transcription factor YAP1 Saccharomyces cerevisiae S288C 30-34 18199679-9 2008 We report that celastrol"s biological effects, including inhibition of glucocorticoid receptor activity, can be blocked by the addition of excess free thiol, suggesting a chemical mechanism for biological activity based on modification of key reactive thiols by this natural product. celastrol 15-24 nuclear receptor subfamily 3 group C member 1 Homo sapiens 71-94 18160842-0 2007 Celastrol inhibits production of nitric oxide and proinflammatory cytokines through MAPK signal transduction and NF-kappaB in LPS-stimulated BV-2 microglial cells. celastrol 0-9 mitogen-activated protein kinase 1 Mus musculus 84-88 18160842-0 2007 Celastrol inhibits production of nitric oxide and proinflammatory cytokines through MAPK signal transduction and NF-kappaB in LPS-stimulated BV-2 microglial cells. celastrol 0-9 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 113-122 18160842-2 2007 Here, we investigated whether celastrol, which has been used as a potent anti-inflammatory and anti-oxidative agent in Chinese medicine, attenuates excessive production of NO and proinflammatory cytokines such as TNF-alpha and IL-1betal in LPS-stimulated BV-2 cells, a mouse microglial cell line. celastrol 30-39 tumor necrosis factor Mus musculus 213-222 18160842-2 2007 Here, we investigated whether celastrol, which has been used as a potent anti-inflammatory and anti-oxidative agent in Chinese medicine, attenuates excessive production of NO and proinflammatory cytokines such as TNF-alpha and IL-1betal in LPS-stimulated BV-2 cells, a mouse microglial cell line. celastrol 30-39 interleukin 1 complex Mus musculus 227-231 18160842-3 2007 We report here that the LPS-elicited excessive production of NO, TNF-alpha, and IL-1beta in BV-2 cells was largely inhibited in the presence of celastrol, and the attenuation of inducible iNOS and these cytokines resulted from the reduced expression of mRNAs of iNOS and these cytokines, respectively. celastrol 144-153 tumor necrosis factor Mus musculus 65-74 18160842-3 2007 We report here that the LPS-elicited excessive production of NO, TNF-alpha, and IL-1beta in BV-2 cells was largely inhibited in the presence of celastrol, and the attenuation of inducible iNOS and these cytokines resulted from the reduced expression of mRNAs of iNOS and these cytokines, respectively. celastrol 144-153 interleukin 1 beta Mus musculus 80-88 18160842-4 2007 The molecular mechanisms that underlie celastrol-mediated attenuation were the inhibition of LPS-induced phosphorylation of MAPK/ERK1/2 and the DNA binding activity of NF-kappaB in BV-2 cells. celastrol 39-48 mitogen-activated protein kinase 1 Mus musculus 124-128 18160842-4 2007 The molecular mechanisms that underlie celastrol-mediated attenuation were the inhibition of LPS-induced phosphorylation of MAPK/ERK1/2 and the DNA binding activity of NF-kappaB in BV-2 cells. celastrol 39-48 mitogen-activated protein kinase 3 Mus musculus 129-135 18160842-4 2007 The molecular mechanisms that underlie celastrol-mediated attenuation were the inhibition of LPS-induced phosphorylation of MAPK/ERK1/2 and the DNA binding activity of NF-kappaB in BV-2 cells. celastrol 39-48 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 168-177 18160842-5 2007 The results indicate that celastrol effectively attenuated NO and proinflammatory cytokine production via the inhibition of ERK1/2 phosphorylation and NF-kappaB activation in LPS-activated microglia. celastrol 26-35 mitogen-activated protein kinase 3 Mus musculus 124-130 18160842-5 2007 The results indicate that celastrol effectively attenuated NO and proinflammatory cytokine production via the inhibition of ERK1/2 phosphorylation and NF-kappaB activation in LPS-activated microglia. celastrol 26-35 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 151-160 16929507-6 2007 Tripterine decreased urine protein excretion and the level of serum anti-dsDNA antibodies and also suppressed the expression of collagen type IV and TGF-beta1 mRNA in the murine kidney tissue. celastrol 0-10 transforming growth factor, beta 1 Mus musculus 149-158 17498488-5 2007 RESULTS: ATRA caused remarkable elevation of intercellular adhesion molecule-1 (ICAM-1) in NB4 cells, which could be significantly reduced by tripterine (P<0.01). celastrol 142-152 intercellular adhesion molecule 1 Homo sapiens 45-78 16929507-0 2007 Effects of tripterine on mRNA expression of TGF-beta1 and collagen IV expression in BW F1 mice. celastrol 11-21 transforming growth factor, beta 1 Mus musculus 44-53 16929507-0 2007 Effects of tripterine on mRNA expression of TGF-beta1 and collagen IV expression in BW F1 mice. celastrol 11-21 WD repeat and FYVE domain containing 3 Mus musculus 84-89 17498488-5 2007 RESULTS: ATRA caused remarkable elevation of intercellular adhesion molecule-1 (ICAM-1) in NB4 cells, which could be significantly reduced by tripterine (P<0.01). celastrol 142-152 intercellular adhesion molecule 1 Homo sapiens 80-86 17498488-6 2007 The expressions of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and ICAM-1 in HUVEC were elevated by conditioned medium from ATRA-induced NB4 (ATRA-NB4-CM) (P<0.01), and inhibited by tripterine with inhibition rates being 25.3%, 42.4% and 61.0% respectively. celastrol 196-206 selectin E Homo sapiens 19-29 17498488-6 2007 The expressions of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and ICAM-1 in HUVEC were elevated by conditioned medium from ATRA-induced NB4 (ATRA-NB4-CM) (P<0.01), and inhibited by tripterine with inhibition rates being 25.3%, 42.4% and 61.0% respectively. celastrol 196-206 vascular cell adhesion molecule 1 Homo sapiens 66-72 17498488-6 2007 The expressions of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and ICAM-1 in HUVEC were elevated by conditioned medium from ATRA-induced NB4 (ATRA-NB4-CM) (P<0.01), and inhibited by tripterine with inhibition rates being 25.3%, 42.4% and 61.0% respectively. celastrol 196-206 intercellular adhesion molecule 1 Homo sapiens 78-84 16984800-0 2006 Inhibition of NF-kappa B activation through targeting I kappa B kinase by celastrol, a quinone methide triterpenoid. celastrol 74-83 nuclear factor kappa B subunit 1 Homo sapiens 14-24 16984800-4 2006 Importantly, celastrol inhibited IKK activity and the constitutively active IKK beta activity in a dose-dependent manner without either affecting the NF-kappa B activation induced by RelA over-expression or directly suppressing the DNA-binding of activated NF-kappa B. celastrol 13-22 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 33-36 16984800-3 2006 Preincubation of celastrol completely blocked the LPS-, TNF-alpha-, or PMA-induced degradation and phosphorylation of I kappa B alpha. celastrol 17-26 tumor necrosis factor Homo sapiens 56-65 16984800-4 2006 Importantly, celastrol inhibited IKK activity and the constitutively active IKK beta activity in a dose-dependent manner without either affecting the NF-kappa B activation induced by RelA over-expression or directly suppressing the DNA-binding of activated NF-kappa B. celastrol 13-22 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 76-84 16984800-3 2006 Preincubation of celastrol completely blocked the LPS-, TNF-alpha-, or PMA-induced degradation and phosphorylation of I kappa B alpha. celastrol 17-26 NFKB inhibitor alpha Homo sapiens 118-133 16984800-4 2006 Importantly, celastrol inhibited IKK activity and the constitutively active IKK beta activity in a dose-dependent manner without either affecting the NF-kappa B activation induced by RelA over-expression or directly suppressing the DNA-binding of activated NF-kappa B. celastrol 13-22 nuclear factor kappa B subunit 1 Homo sapiens 257-267 16984800-5 2006 However, mutation of cysteine 179 in the activation loop of IKK beta abolished sensitivity towards to celastrol, suggesting that celastrol suppressed the NF-kappa B activation by targeting cysteine 179 in the IKK. celastrol 102-111 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 60-68 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 intercellular adhesion molecule 1 Homo sapiens 298-331 16984800-5 2006 However, mutation of cysteine 179 in the activation loop of IKK beta abolished sensitivity towards to celastrol, suggesting that celastrol suppressed the NF-kappa B activation by targeting cysteine 179 in the IKK. celastrol 102-111 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 60-63 16984800-5 2006 However, mutation of cysteine 179 in the activation loop of IKK beta abolished sensitivity towards to celastrol, suggesting that celastrol suppressed the NF-kappa B activation by targeting cysteine 179 in the IKK. celastrol 129-138 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 60-68 16984800-5 2006 However, mutation of cysteine 179 in the activation loop of IKK beta abolished sensitivity towards to celastrol, suggesting that celastrol suppressed the NF-kappa B activation by targeting cysteine 179 in the IKK. celastrol 129-138 nuclear factor kappa B subunit 1 Homo sapiens 154-164 16984800-5 2006 However, mutation of cysteine 179 in the activation loop of IKK beta abolished sensitivity towards to celastrol, suggesting that celastrol suppressed the NF-kappa B activation by targeting cysteine 179 in the IKK. celastrol 129-138 inhibitor of nuclear factor kappa B kinase subunit beta Homo sapiens 60-63 16984800-6 2006 To verify that celastrol is a NF-kappa B inhibitor, we investigated its effect on some NF-kappa B target genes expressions. celastrol 15-24 nuclear factor kappa B subunit 1 Homo sapiens 30-40 16984800-6 2006 To verify that celastrol is a NF-kappa B inhibitor, we investigated its effect on some NF-kappa B target genes expressions. celastrol 15-24 nuclear factor kappa B subunit 1 Homo sapiens 87-97 16984800-7 2006 Celastrol prevented not only LPS-induced mRNA expression of iNOS and TNF-alpha, but also TNF-alpha-induced Bfl-1/A1 expression, a prosurvival Bcl-2 homologue. celastrol 0-9 nitric oxide synthase 2 Homo sapiens 60-64 16984800-7 2006 Celastrol prevented not only LPS-induced mRNA expression of iNOS and TNF-alpha, but also TNF-alpha-induced Bfl-1/A1 expression, a prosurvival Bcl-2 homologue. celastrol 0-9 tumor necrosis factor Homo sapiens 69-78 16984800-7 2006 Celastrol prevented not only LPS-induced mRNA expression of iNOS and TNF-alpha, but also TNF-alpha-induced Bfl-1/A1 expression, a prosurvival Bcl-2 homologue. celastrol 0-9 tumor necrosis factor Homo sapiens 89-98 16984800-7 2006 Celastrol prevented not only LPS-induced mRNA expression of iNOS and TNF-alpha, but also TNF-alpha-induced Bfl-1/A1 expression, a prosurvival Bcl-2 homologue. celastrol 0-9 BCL2 related protein A1 Homo sapiens 107-112 16984800-7 2006 Celastrol prevented not only LPS-induced mRNA expression of iNOS and TNF-alpha, but also TNF-alpha-induced Bfl-1/A1 expression, a prosurvival Bcl-2 homologue. celastrol 0-9 BCL2 apoptosis regulator Homo sapiens 142-147 16984800-8 2006 Consistent with these results, celastrol significantly suppressed the production of NO and TNF-alpha in LPS-stimulated RAW264.7 cells, and increased the cytotoxicity of TNF-alpha in HT-1080 cells. celastrol 31-40 tumor necrosis factor Mus musculus 91-100 16984800-8 2006 Consistent with these results, celastrol significantly suppressed the production of NO and TNF-alpha in LPS-stimulated RAW264.7 cells, and increased the cytotoxicity of TNF-alpha in HT-1080 cells. celastrol 31-40 tumor necrosis factor Mus musculus 169-178 16984800-10 2006 Taken together, this study extends our understanding on the molecular mechanisms underlying the anti-inflammatory and anti-cancer activities of celastrol and celastrol-containing medicinal plant, which would be a valuable candidate for the intervention of NF-kappa B-dependent pathological conditions. celastrol 144-153 nuclear factor kappa B subunit 1 Homo sapiens 256-266 16984800-10 2006 Taken together, this study extends our understanding on the molecular mechanisms underlying the anti-inflammatory and anti-cancer activities of celastrol and celastrol-containing medicinal plant, which would be a valuable candidate for the intervention of NF-kappa B-dependent pathological conditions. celastrol 158-167 nuclear factor kappa B subunit 1 Homo sapiens 256-266 17010675-5 2006 Validating this prediction, we demonstrate that celastrol and gedunin inhibit HSP90 activity and HSP90 clients, including AR. celastrol 48-57 heat shock protein 90 alpha family class A member 1 Homo sapiens 78-83 17010675-5 2006 Validating this prediction, we demonstrate that celastrol and gedunin inhibit HSP90 activity and HSP90 clients, including AR. celastrol 48-57 heat shock protein 90 alpha family class A member 1 Homo sapiens 97-102 17010675-5 2006 Validating this prediction, we demonstrate that celastrol and gedunin inhibit HSP90 activity and HSP90 clients, including AR. celastrol 48-57 androgen receptor Homo sapiens 122-124 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 tumor necrosis factor Homo sapiens 75-102 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 tumor necrosis factor Homo sapiens 104-113 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 selectin E Homo sapiens 232-242 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 cell adhesion molecule 1 Homo sapiens 253-283 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 vascular cell adhesion molecule 1 Homo sapiens 285-291 16769766-4 2006 In the present study, we show that in inflammatory conditions, mimicked by tumor necrosis factor alpha (TNF-alpha) stimulation, pretreatment for 6 h with tripterine at nontoxic concentrations of 20-200 nM inhibits the expression of E-selectin, vascular cell adhesion molecule (CAM)-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner. celastrol 154-164 intercellular adhesion molecule 1 Homo sapiens 333-339 16769766-5 2006 Tripterine (200 nM) almost completely inhibits expression of VCAM-1 [50% inhibitory concentration (IC50) = 52 nM] and ICAM-1 (IC50 = 51 nM) and 73% of E-selectin (IC50 = 94 nM). celastrol 0-10 vascular cell adhesion molecule 1 Homo sapiens 61-67 16769766-5 2006 Tripterine (200 nM) almost completely inhibits expression of VCAM-1 [50% inhibitory concentration (IC50) = 52 nM] and ICAM-1 (IC50 = 51 nM) and 73% of E-selectin (IC50 = 94 nM). celastrol 0-10 intercellular adhesion molecule 1 Homo sapiens 118-124 16769766-5 2006 Tripterine (200 nM) almost completely inhibits expression of VCAM-1 [50% inhibitory concentration (IC50) = 52 nM] and ICAM-1 (IC50 = 51 nM) and 73% of E-selectin (IC50 = 94 nM). celastrol 0-10 selectin E Homo sapiens 151-161 16769766-7 2006 Effects on endothelial CAM of other proinflammatory cytokines, such as interleukin-1beta and interferon-gamma, were also inhibited significantly by tripterine. celastrol 148-158 interleukin 1 beta Homo sapiens 71-88 16769766-7 2006 Effects on endothelial CAM of other proinflammatory cytokines, such as interleukin-1beta and interferon-gamma, were also inhibited significantly by tripterine. celastrol 148-158 interferon gamma Homo sapiens 93-109 16769766-9 2006 In addition, tripterine inhibited adhesion of human monocytes and T lymphocytes to TNF-alpha-stimulated HUVEC. celastrol 13-23 tumor necrosis factor Homo sapiens 83-92 16769766-10 2006 Finally, tripterine inhibited TNF-alpha-driven CAM mRNA transcription and nuclear factor-kappaB nuclear (NF-kappaB) translocation. celastrol 9-19 tumor necrosis factor Homo sapiens 30-39 16092942-8 2005 Celastrol induced heat shock protein 70 within dopaminergic neurons and decreased tumor necrosis factor-alpha and nuclear factor kappa B immunostainings as well as astrogliosis. celastrol 0-9 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 18-39 16407206-0 2006 Chronic inhibition of cardiac Kir2.1 and HERG potassium channels by celastrol with dual effects on both ion conductivity and protein trafficking. celastrol 68-77 potassium voltage-gated channel subfamily H member 2 Homo sapiens 41-45 16407206-5 2006 Further investigation of celastrol (3-hydroxy-24-nor-2-oxo-1 (10),3,5,7-friedelatetraen-29-oic acid), a cell-permeable dienonephenolic triterpene compound, revealed its potent inhibitory activity on both Kir2.1 and hERG potassium channels, causal to QT prolongation. celastrol 25-34 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 204-210 16407206-5 2006 Further investigation of celastrol (3-hydroxy-24-nor-2-oxo-1 (10),3,5,7-friedelatetraen-29-oic acid), a cell-permeable dienonephenolic triterpene compound, revealed its potent inhibitory activity on both Kir2.1 and hERG potassium channels, causal to QT prolongation. celastrol 25-34 ETS transcription factor ERG Homo sapiens 215-219 16651429-7 2006 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or LNCaP (AR-positive) cells results in the accumulation of ubiquitinated proteins and three natural proteasome substrates (IkappaB-alpha, Bax, and p27), accompanied by suppression of AR protein expression (in LNCaP cells) and induction of apoptosis. celastrol 41-50 chromobox 8 Homo sapiens 54-58 16651429-7 2006 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or LNCaP (AR-positive) cells results in the accumulation of ubiquitinated proteins and three natural proteasome substrates (IkappaB-alpha, Bax, and p27), accompanied by suppression of AR protein expression (in LNCaP cells) and induction of apoptosis. celastrol 41-50 NFKB inhibitor alpha Homo sapiens 219-232 16651429-7 2006 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or LNCaP (AR-positive) cells results in the accumulation of ubiquitinated proteins and three natural proteasome substrates (IkappaB-alpha, Bax, and p27), accompanied by suppression of AR protein expression (in LNCaP cells) and induction of apoptosis. celastrol 41-50 BCL2 associated X, apoptosis regulator Homo sapiens 234-237 16651429-7 2006 Inhibition of the proteasome activity by Celastrol in PC-3 (androgen receptor- or AR-negative) or LNCaP (AR-positive) cells results in the accumulation of ubiquitinated proteins and three natural proteasome substrates (IkappaB-alpha, Bax, and p27), accompanied by suppression of AR protein expression (in LNCaP cells) and induction of apoptosis. celastrol 41-50 interferon alpha inducible protein 27 Homo sapiens 243-246 16651429-8 2006 Treatment of PC-3 tumor-bearing nude mice with Celastrol (1-3 mg/kg/d, i.p., 1-31 days) resulted in significant inhibition (65-93%) of the tumor growth. celastrol 47-56 chromobox 8 Mus musculus 13-17 16407206-0 2006 Chronic inhibition of cardiac Kir2.1 and HERG potassium channels by celastrol with dual effects on both ion conductivity and protein trafficking. celastrol 68-77 potassium inwardly rectifying channel subfamily J member 2 Homo sapiens 30-36 16092942-8 2005 Celastrol induced heat shock protein 70 within dopaminergic neurons and decreased tumor necrosis factor-alpha and nuclear factor kappa B immunostainings as well as astrogliosis. celastrol 0-9 tumor necrosis factor Rattus norvegicus 82-109 15509580-4 2004 From a structure/function examination, the celastrol structure is remarkably specific and activates heat shock transcription factor 1 (HSF1) with kinetics similar to those of heat stress, as determined by the induction of HSF1 DNA binding, hyperphosphorylation of HSF1, and expression of chaperone genes. celastrol 43-52 heat shock transcription factor 1 Homo sapiens 100-133 16909005-8 2005 Celastrol treatment reduced TNF-alpha, iNOS, CD40, and GFAP immunoreactivity in the lumbar spinal cord sections of celastrol-treated G93A mice compared to untreated G93A mice. celastrol 0-9 tumor necrosis factor Mus musculus 28-37 16909005-8 2005 Celastrol treatment reduced TNF-alpha, iNOS, CD40, and GFAP immunoreactivity in the lumbar spinal cord sections of celastrol-treated G93A mice compared to untreated G93A mice. celastrol 0-9 nitric oxide synthase 2, inducible Mus musculus 39-43 16909005-8 2005 Celastrol treatment reduced TNF-alpha, iNOS, CD40, and GFAP immunoreactivity in the lumbar spinal cord sections of celastrol-treated G93A mice compared to untreated G93A mice. celastrol 0-9 CD40 antigen Mus musculus 45-49 16909005-8 2005 Celastrol treatment reduced TNF-alpha, iNOS, CD40, and GFAP immunoreactivity in the lumbar spinal cord sections of celastrol-treated G93A mice compared to untreated G93A mice. celastrol 0-9 glial fibrillary acidic protein Mus musculus 55-59 16909005-8 2005 Celastrol treatment reduced TNF-alpha, iNOS, CD40, and GFAP immunoreactivity in the lumbar spinal cord sections of celastrol-treated G93A mice compared to untreated G93A mice. celastrol 115-124 glial fibrillary acidic protein Mus musculus 55-59 16909005-10 2005 HSP70 immunoreactivity was increased in lumbar spinal cord neurons of celastrol-treated G93A mice. celastrol 70-79 heat shock protein 1B Mus musculus 0-5 15840409-4 2005 Treatment with tripterine 12 mg kg(-1) day(-1) for 15 days protected renal from glomerular injury with a concomitant reduction of serum autoantibodies and total immunoglobulin G (IgG) also with a improvement of splenocyte proliferation stimulated with concanavalin A and lipopolysaccharide. celastrol 15-25 immunoglobulin heavy variable V1-62 Mus musculus 161-177 15840409-4 2005 Treatment with tripterine 12 mg kg(-1) day(-1) for 15 days protected renal from glomerular injury with a concomitant reduction of serum autoantibodies and total immunoglobulin G (IgG) also with a improvement of splenocyte proliferation stimulated with concanavalin A and lipopolysaccharide. celastrol 15-25 immunoglobulin heavy variable V1-62 Mus musculus 179-182 15649316-8 2005 Of these, both juglone and celastrol were effective in reversing the abnormal cellular localization of full-length mutant huntingtin observed in mutant HdhQ111/Q111 striatal cells. celastrol 27-36 huntingtin Mus musculus 122-132 15509580-4 2004 From a structure/function examination, the celastrol structure is remarkably specific and activates heat shock transcription factor 1 (HSF1) with kinetics similar to those of heat stress, as determined by the induction of HSF1 DNA binding, hyperphosphorylation of HSF1, and expression of chaperone genes. celastrol 43-52 heat shock transcription factor 1 Homo sapiens 135-139 15509580-4 2004 From a structure/function examination, the celastrol structure is remarkably specific and activates heat shock transcription factor 1 (HSF1) with kinetics similar to those of heat stress, as determined by the induction of HSF1 DNA binding, hyperphosphorylation of HSF1, and expression of chaperone genes. celastrol 43-52 heat shock transcription factor 1 Homo sapiens 222-226 15509580-4 2004 From a structure/function examination, the celastrol structure is remarkably specific and activates heat shock transcription factor 1 (HSF1) with kinetics similar to those of heat stress, as determined by the induction of HSF1 DNA binding, hyperphosphorylation of HSF1, and expression of chaperone genes. celastrol 43-52 heat shock transcription factor 1 Homo sapiens 222-226 12133425-2 2002 METHODS: Different doses of Tripterine were injected peritoneally to BW F1 mice at different stages. celastrol 28-38 WD repeat and FYVE domain containing 3 Mus musculus 69-74 15130326-9 2004 In vitro, the concentration of histamine and eotaxin in coculture supernants and the expression of SCF protein in fibroblasts from coculture were (3.83 +/- 0.41) ng/ml, (5.79 +/- 0.40) ng/ml and (95 +/- 3)%, respectively; after tripterine intervention, the data changed to (2.88 +/- 0.35) ng/ml, (4.24 +/- 0.29) ng/ml, (17 +/- 5)% (all P < 0.01). celastrol 228-238 kit ligand Mus musculus 99-102 15130326-10 2004 CONCLUSIONS: Tripterine might suppress airway inflammation in asthmatic mice, probably by downregulating the expression of SCF in fibroblasts, then inhibiting the production of histamine and eotaxin in mast cells. celastrol 13-23 kit ligand Mus musculus 123-126 15130326-10 2004 CONCLUSIONS: Tripterine might suppress airway inflammation in asthmatic mice, probably by downregulating the expression of SCF in fibroblasts, then inhibiting the production of histamine and eotaxin in mast cells. celastrol 13-23 chemokine (C-C motif) ligand 11 Mus musculus 191-198 14640511-4 2003 The major terpenoid components, celastrol (6) and its methyl ester derivative, pristimerin (7), were significantly active against nine cancer cell lines, including A549, MCF-7, HCT-8, KB, KB-VIN, U-87-MG, PC-3, 1A9, and PTX10 cell lines, with ED(50) values ranging from 0.076 to 0.34 microg/mL. celastrol 32-41 long intergenic non-protein coding RNA 1191 Homo sapiens 191-194 12508653-4 2002 Immunohistochemistry was used to examine the expression of Bax, Bcl-2 after treatment of triptolide and celastrol. celastrol 104-113 BCL2 apoptosis regulator Homo sapiens 64-69 12508653-7 2002 CONCLUSION: Triptolide and celastrol inhibit the proliferation of glioma cells in vitro, which was associated with promoting the expression of Bax and inhibiting the expression of Bcl-2 and accelerating cell apotosis. celastrol 27-36 BCL2 associated X, apoptosis regulator Homo sapiens 143-146 12508653-7 2002 CONCLUSION: Triptolide and celastrol inhibit the proliferation of glioma cells in vitro, which was associated with promoting the expression of Bax and inhibiting the expression of Bcl-2 and accelerating cell apotosis. celastrol 27-36 BCL2 apoptosis regulator Homo sapiens 180-185 12133425-4 2002 RESULTS: (1) Tripterine suppressed the development of proteinuria, decreased the level of serum anti-dsDNA antibodies, reduced the expressions of collagen type IV, fibronectin, TIMP-1, TIMP-2, TGF-beta(1) and improved the expressions of MMP-1, -2 in the murine kidney. celastrol 13-23 fibronectin 1 Mus musculus 164-175 12133425-4 2002 RESULTS: (1) Tripterine suppressed the development of proteinuria, decreased the level of serum anti-dsDNA antibodies, reduced the expressions of collagen type IV, fibronectin, TIMP-1, TIMP-2, TGF-beta(1) and improved the expressions of MMP-1, -2 in the murine kidney. celastrol 13-23 tissue inhibitor of metalloproteinase 1 Mus musculus 177-183 12133425-4 2002 RESULTS: (1) Tripterine suppressed the development of proteinuria, decreased the level of serum anti-dsDNA antibodies, reduced the expressions of collagen type IV, fibronectin, TIMP-1, TIMP-2, TGF-beta(1) and improved the expressions of MMP-1, -2 in the murine kidney. celastrol 13-23 tissue inhibitor of metalloproteinase 2 Mus musculus 185-191 12133425-4 2002 RESULTS: (1) Tripterine suppressed the development of proteinuria, decreased the level of serum anti-dsDNA antibodies, reduced the expressions of collagen type IV, fibronectin, TIMP-1, TIMP-2, TGF-beta(1) and improved the expressions of MMP-1, -2 in the murine kidney. celastrol 13-23 transforming growth factor, beta 1 Mus musculus 193-204 12133425-4 2002 RESULTS: (1) Tripterine suppressed the development of proteinuria, decreased the level of serum anti-dsDNA antibodies, reduced the expressions of collagen type IV, fibronectin, TIMP-1, TIMP-2, TGF-beta(1) and improved the expressions of MMP-1, -2 in the murine kidney. celastrol 13-23 matrix metallopeptidase 13 Mus musculus 237-242 11601243-9 1999 Tripterine could upregulate Bax, c-myc expression and downregulate bcl-2 expression at protein level. celastrol 0-10 BCL2 associated X, apoptosis regulator Homo sapiens 28-31 11513350-5 2001 In low nanomolar concentrations celastrol was found to suppress the production by human monocytes and macrophages of the pro-inflammatory cytokines TNF-alpha and IL-1beta. celastrol 32-41 tumor necrosis factor Homo sapiens 148-157 11513350-5 2001 In low nanomolar concentrations celastrol was found to suppress the production by human monocytes and macrophages of the pro-inflammatory cytokines TNF-alpha and IL-1beta. celastrol 32-41 interleukin 1 alpha Homo sapiens 162-170 11601243-9 1999 Tripterine could upregulate Bax, c-myc expression and downregulate bcl-2 expression at protein level. celastrol 0-10 MYC proto-oncogene, bHLH transcription factor Homo sapiens 33-38 11601243-9 1999 Tripterine could upregulate Bax, c-myc expression and downregulate bcl-2 expression at protein level. celastrol 0-10 BCL2 apoptosis regulator Homo sapiens 67-72 11601243-10 1999 CONCLUSION: Tripterine can efficiently induce HMC-1 cell apoptosis, occurring mainly in S phase, which is correlated with upregulating Bax, c-myc expression and downregulating bcl-2 expression. celastrol 12-22 BCL2 associated X, apoptosis regulator Homo sapiens 135-138 11601243-10 1999 CONCLUSION: Tripterine can efficiently induce HMC-1 cell apoptosis, occurring mainly in S phase, which is correlated with upregulating Bax, c-myc expression and downregulating bcl-2 expression. celastrol 12-22 MYC proto-oncogene, bHLH transcription factor Homo sapiens 140-145 11601243-10 1999 CONCLUSION: Tripterine can efficiently induce HMC-1 cell apoptosis, occurring mainly in S phase, which is correlated with upregulating Bax, c-myc expression and downregulating bcl-2 expression. celastrol 12-22 BCL2 apoptosis regulator Homo sapiens 176-181 11367666-0 1998 [Effect of Tripterine on mRNA expression of c-myc and platelet derived growth factor of vascular smooth muscle cell in rats]. celastrol 11-21 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 44-49 9873452-2 1998 Tripterine and closely related triterpenoid derivatives as IL-1 beta release inhibitors are discussed. celastrol 0-10 interleukin 1 beta Homo sapiens 59-68 9934491-2 1998 Truncated analogs of tripterine as cytokine (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and IL-8) release inhibitors are discussed. celastrol 21-31 interleukin 1 alpha Homo sapiens 45-55 9934491-2 1998 Truncated analogs of tripterine as cytokine (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and IL-8) release inhibitors are discussed. celastrol 21-31 interleukin 1 beta Homo sapiens 57-66 9934491-2 1998 Truncated analogs of tripterine as cytokine (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and IL-8) release inhibitors are discussed. celastrol 21-31 tumor necrosis factor Homo sapiens 68-77 9934491-2 1998 Truncated analogs of tripterine as cytokine (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and IL-8) release inhibitors are discussed. celastrol 21-31 interleukin 6 Homo sapiens 79-83 9934491-2 1998 Truncated analogs of tripterine as cytokine (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, and IL-8) release inhibitors are discussed. celastrol 21-31 C-X-C motif chemokine ligand 8 Homo sapiens 89-93 11367666-1 1998 OBJECTIVE: To observe the effect of Tripterine on mRNA expression of c-myc and platelet derived growth factor (PDGF) in vascular smooth muscle cell (VSMC) of rats. celastrol 36-46 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 69-74 11367666-6 1998 RESULTS: Tripterine inhibited the PDGF mRNA expression of VSMC and decreased c-myc mRNA expression in a dose-dependent manner, either vs. control. celastrol 9-19 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 77-82 11367666-7 1998 CONCLUSION: Tripterine could inhibit mRNA expression of c-myc and PDGF in VSMC, therefore, it would inhibit overproliferation of VSMC. celastrol 12-22 MYC proto-oncogene, bHLH transcription factor Rattus norvegicus 56-61 1821082-0 1991 [Inhibitory effect of tripterine on activities of IL-1, IL-2 and release of PGE2]. celastrol 22-32 interleukin 1 complex Mus musculus 50-54 1821082-0 1991 [Inhibitory effect of tripterine on activities of IL-1, IL-2 and release of PGE2]. celastrol 22-32 interleukin 2 Mus musculus 56-60 1821082-4 1991 The results showed that tripterine (0.1-1.0 microgram/ml) significantly inhibited IL-1 activity of murine peritoneal macrophages induced by LPS. celastrol 24-34 interleukin 1 complex Mus musculus 82-86 1821082-5 1991 Because both intracellular and extracellular IL-1 activities were decreased, so tripterine might be able to reduce the production and release of IL-1. celastrol 80-90 interleukin 1 complex Mus musculus 45-49 1821082-5 1991 Because both intracellular and extracellular IL-1 activities were decreased, so tripterine might be able to reduce the production and release of IL-1. celastrol 80-90 interleukin 1 complex Mus musculus 145-149 1821082-6 1991 Besides, inhibition of IL-1 production was observed when macrophages were pretreated with the drug for 8 h and 16 h. A good relationship was found between the effect and concentration of tripterine which inhibited IL-2 production from ConA-activated murine splenocytes. celastrol 187-197 interleukin 1 complex Mus musculus 23-27 1821082-6 1991 Besides, inhibition of IL-1 production was observed when macrophages were pretreated with the drug for 8 h and 16 h. A good relationship was found between the effect and concentration of tripterine which inhibited IL-2 production from ConA-activated murine splenocytes. celastrol 187-197 interleukin 2 Mus musculus 214-218 33945201-0 2021 Celastrol inhibit the proliferation, invasion and migration of human cervical HeLa cancer cells through down-regulation of MMP-2 and MMP-9. celastrol 0-9 matrix metallopeptidase 2 Homo sapiens 123-128 33945201-0 2021 Celastrol inhibit the proliferation, invasion and migration of human cervical HeLa cancer cells through down-regulation of MMP-2 and MMP-9. celastrol 0-9 matrix metallopeptidase 9 Homo sapiens 133-138 33945201-1 2021 The present study evaluated the anticancer potential of celastrol through down-regulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. celastrol 56-65 matrix metallopeptidase 2 Homo sapiens 93-119 33945201-1 2021 The present study evaluated the anticancer potential of celastrol through down-regulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. celastrol 56-65 matrix metallopeptidase 2 Homo sapiens 121-126 33945201-1 2021 The present study evaluated the anticancer potential of celastrol through down-regulation of matrix metalloproteinase-2 (MMP-2) and MMP-9. celastrol 56-65 matrix metallopeptidase 9 Homo sapiens 132-137 33945201-5 2021 In addition, the expression level of MMP-2, MMP-9 and caspase-3 was evaluated following celastrol treatment. celastrol 88-97 matrix metallopeptidase 2 Homo sapiens 37-42 33945201-5 2021 In addition, the expression level of MMP-2, MMP-9 and caspase-3 was evaluated following celastrol treatment. celastrol 88-97 caspase 3 Homo sapiens 54-63 33945201-9 2021 Reduced expression of MMP-2 and MMP-9 and increased expression of caspase-3 were observed following celastrol treatment. celastrol 100-109 matrix metallopeptidase 2 Homo sapiens 22-27 33945201-9 2021 Reduced expression of MMP-2 and MMP-9 and increased expression of caspase-3 were observed following celastrol treatment. celastrol 100-109 matrix metallopeptidase 9 Homo sapiens 32-37 33945201-9 2021 Reduced expression of MMP-2 and MMP-9 and increased expression of caspase-3 were observed following celastrol treatment. celastrol 100-109 caspase 3 Homo sapiens 66-75 34742058-0 2022 Glucose transporter 1 (GLUT1)-targeting and hypoxia-activated mitochondria-specific chemo-thermal therapy via a glycosylated poly(amido amine)/celastrol (PAMAM/Cel) complex. celastrol 143-152 solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus 0-21 33808393-0 2021 Celastrol Prevents Oxidative Stress Effects on FSHR, PAPP, and CYP19A1 Gene Expression in Cultured Human Granulosa-Lutein Cells. celastrol 0-9 follicle stimulating hormone receptor Homo sapiens 47-51 33808393-0 2021 Celastrol Prevents Oxidative Stress Effects on FSHR, PAPP, and CYP19A1 Gene Expression in Cultured Human Granulosa-Lutein Cells. celastrol 0-9 cytochrome P450 family 19 subfamily A member 1 Homo sapiens 63-70 33808393-9 2021 In addition to the antioxidant activity, celastrol may well have an independent role on regulation of gene expression in hGL cells. celastrol 41-50 LLGL scribble cell polarity complex component 2 Homo sapiens 121-124 25660987-6 2015 Furthermore, Celastrol limited the production of Th17-differentiating cytokines and chemokines (CCL3, CCL5). celastrol 13-22 C-C motif chemokine ligand 3 Rattus norvegicus 96-100 25660987-6 2015 Furthermore, Celastrol limited the production of Th17-differentiating cytokines and chemokines (CCL3, CCL5). celastrol 13-22 C-C motif chemokine ligand 5 Rattus norvegicus 102-106 34742058-0 2022 Glucose transporter 1 (GLUT1)-targeting and hypoxia-activated mitochondria-specific chemo-thermal therapy via a glycosylated poly(amido amine)/celastrol (PAMAM/Cel) complex. celastrol 143-152 solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus 23-28 34510370-0 2022 Celastrol attenuates chronic constrictive injury-induced neuropathic pain and inhibits the TLR4/NF-kappaB signaling pathway in the spinal cord. celastrol 0-9 toll-like receptor 4 Rattus norvegicus 91-95 34968902-0 2022 Synthesis and biological evaluation of celastrol derivatives as potential anti-glioma agents by activating RIP1/RIP3/MLKL pathway to induce necroptosis. celastrol 39-48 receptor interacting serine/threonine kinase 1 Homo sapiens 107-111 34968902-0 2022 Synthesis and biological evaluation of celastrol derivatives as potential anti-glioma agents by activating RIP1/RIP3/MLKL pathway to induce necroptosis. celastrol 39-48 myosin phosphatase Rho interacting protein Homo sapiens 112-116 34968902-0 2022 Synthesis and biological evaluation of celastrol derivatives as potential anti-glioma agents by activating RIP1/RIP3/MLKL pathway to induce necroptosis. celastrol 39-48 mixed lineage kinase domain like pseudokinase Homo sapiens 117-121 34958783-7 2022 In the present study, we investigated the effect of four major components of TWHF, i.e. Triptolide (TPL), Celastrol (CL), and two alkaloids Wilforine (WFR) and Wilforgine (WFG) on the function of OATP1B1. celastrol 106-115 solute carrier organic anion transporter family member 1B1 Homo sapiens 196-203 34510370-10 2022 Additionally, the levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 1beta and interleukin 6, detected by ELISA in the spinal cord of the rats with NP, were significantly inhibited by celastrol. celastrol 226-235 tumor necrosis factor Rattus norvegicus 87-96 34510370-10 2022 Additionally, the levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 1beta and interleukin 6, detected by ELISA in the spinal cord of the rats with NP, were significantly inhibited by celastrol. celastrol 226-235 interleukin 1 beta Rattus norvegicus 99-116 34510370-10 2022 Additionally, the levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 1beta and interleukin 6, detected by ELISA in the spinal cord of the rats with NP, were significantly inhibited by celastrol. celastrol 226-235 interleukin 6 Rattus norvegicus 121-134 34510370-11 2022 Furthermore, celastrol treatment dramatically inhibited the expression of the TLR4/NF-kappaB signaling pathway in the spinal cord. celastrol 13-22 toll-like receptor 4 Rattus norvegicus 78-82 34510370-10 2022 Additionally, the levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 1beta and interleukin 6, detected by ELISA in the spinal cord of the rats with NP, were significantly inhibited by celastrol. celastrol 226-235 tumor necrosis factor Rattus norvegicus 58-85 34942974-0 2021 Celastrol and Melatonin Modify SIRT1, SIRT6 and SIRT7 Gene Expression and Improve the Response of Human Granulosa-Lutein Cells to Oxidative Stress. celastrol 0-9 sirtuin 1 Homo sapiens 31-36 34510370-12 2022 Taken together, our findings suggested that celastrol could attenuate mechanical and thermal pain in CCI-induced NP, and this protection might be attributed to inhibiting the TLR4/NF-kappaB signaling pathway and exerting anti-inflammatory effects in the spinal cord. celastrol 44-53 toll-like receptor 4 Rattus norvegicus 175-179 34959287-1 2021 Herein, a flexible oral colon-targeting delivery system, mediated by electrostatic layer-by-layer alternate deposition with pectin-trimethyl chitosan (TMC) onto liposomes-loading celastrol (Cel/PT-LbL Lipo), was fabricated to enhance anti-UC efficacy. celastrol 179-188 carboxyl ester lipase Homo sapiens 190-193 34959287-3 2021 Based on its bilayer coating of polysaccharides, Cel/PT-LbL Lipo alleviated cytotoxicity of celastrol in colon epithelial NCM460 cells. celastrol 92-101 carboxyl ester lipase Homo sapiens 49-52 34560609-9 2021 The exposure of endometriotic cells to TAK1 inhibitor, celastrol caused activation of caspase-3 and -9 that led to PARP cleavage and induced apoptosis. celastrol 55-64 mitogen-activated protein kinase kinase kinase 7 Homo sapiens 39-43 34560609-9 2021 The exposure of endometriotic cells to TAK1 inhibitor, celastrol caused activation of caspase-3 and -9 that led to PARP cleavage and induced apoptosis. celastrol 55-64 caspase 3 Homo sapiens 86-102 34560609-9 2021 The exposure of endometriotic cells to TAK1 inhibitor, celastrol caused activation of caspase-3 and -9 that led to PARP cleavage and induced apoptosis. celastrol 55-64 collagen type XI alpha 2 chain Homo sapiens 115-119 34030574-3 2021 The most potent compounds were found to be oleanic acid, betulinic acid and celastrol with IC50 values of 3.89-5.07 muM, that acted as mixed (uncompetitive plus non-competitive) inhibitors of COMT, representing a new skeleton of COMT inhibitor. celastrol 76-85 catechol-O-methyltransferase Homo sapiens 192-196 34030574-3 2021 The most potent compounds were found to be oleanic acid, betulinic acid and celastrol with IC50 values of 3.89-5.07 muM, that acted as mixed (uncompetitive plus non-competitive) inhibitors of COMT, representing a new skeleton of COMT inhibitor. celastrol 76-85 catechol-O-methyltransferase Homo sapiens 229-233 34942974-0 2021 Celastrol and Melatonin Modify SIRT1, SIRT6 and SIRT7 Gene Expression and Improve the Response of Human Granulosa-Lutein Cells to Oxidative Stress. celastrol 0-9 sirtuin 6 Homo sapiens 38-43 34942974-0 2021 Celastrol and Melatonin Modify SIRT1, SIRT6 and SIRT7 Gene Expression and Improve the Response of Human Granulosa-Lutein Cells to Oxidative Stress. celastrol 0-9 sirtuin 7 Homo sapiens 48-53 34942974-2 2021 SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. celastrol 129-138 sirtuin 1 Homo sapiens 0-5 34942974-2 2021 SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. celastrol 129-138 sirtuin 6 Homo sapiens 7-12 34942974-2 2021 SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. celastrol 129-138 sirtuin 7 Homo sapiens 17-22 34942974-5 2021 In addition, melatonin induced SIRT1, SIRT6 and SIRT7 gene expression while celastrol only induced SIRT7 gene expression. celastrol 76-85 sirtuin 7 Homo sapiens 99-104 34942974-7 2021 Our previous data for cultured hGL cells showed a dual role of celastrol as a free radical scavenger and as a protective agent by regulating gene expression. celastrol 63-72 lipase F, gastric type Homo sapiens 31-34 34942974-8 2021 This study shows a direct effect of celastrol on SIRT7 gene expression. celastrol 36-45 sirtuin 7 Homo sapiens 49-54 34942974-10 2021 In conclusion, our results show increased hGL cells survival with melatonin or celastrol treatment under OS conditions, probably through the regulation of nuclear sirtuins" gene expression. celastrol 79-88 lipase F, gastric type Homo sapiens 42-45 34507130-0 2021 Corrigendum to "Celastrol nanoemulsion induces immunogenicity and downregulates PD-L1 to boost abscopal effect in melanoma therapy" (Biomaterials 269 (2021) 120604). celastrol 16-25 CD274 molecule Homo sapiens 80-85 34304725-0 2021 Topical application of celastrol alleviates atopic dermatitis symptoms mediated through the regulation of thymic stromal lymphopoietin and group 2 innate lymphoid cells. celastrol 23-32 thymic stromal lymphopoietin Mus musculus 106-134 34304725-4 2021 The aim of this study was to investigate whether celastrol alleviated atopic dermatitis symptoms by regulating TSLP expression and ILC2 stimulation. celastrol 49-58 thymic stromal lymphopoietin Mus musculus 111-115 34304725-5 2021 Celastrol suppressed TSLP production in mouse keratinocyte cells by inhibiting NF-kB activation. celastrol 0-9 thymic stromal lymphopoietin Mus musculus 21-25 34304725-7 2021 Celastrol decreased the levels of TSLP in atopic dermatitis skin lesions of HDM-stimulated NC/Nga mice. celastrol 0-9 thymic stromal lymphopoietin Mus musculus 34-38 34304725-8 2021 Celastrol reduced levels of Th2 cytokines including IL-4, IL-5, and IL-13 in atopic dermatitis skin lesions of NC/Nga mice. celastrol 0-9 interleukin 4 Mus musculus 52-56 34304725-8 2021 Celastrol reduced levels of Th2 cytokines including IL-4, IL-5, and IL-13 in atopic dermatitis skin lesions of NC/Nga mice. celastrol 0-9 interleukin 5 Mus musculus 58-62 34304725-8 2021 Celastrol reduced levels of Th2 cytokines including IL-4, IL-5, and IL-13 in atopic dermatitis skin lesions of NC/Nga mice. celastrol 0-9 interleukin 13 Mus musculus 68-73 34304725-10 2021 These results indicate that topical application of celastrol improved atopic dermatitis symptoms by lowering TSLP levels and concomitant immune responses. celastrol 51-60 thymic stromal lymphopoietin Mus musculus 109-113 34256125-0 2021 Synthesis, computational docking and biological evaluation of celastrol derivatives as dual inhibitors of SERCA and P-glycoprotein in cancer therapy. celastrol 62-71 ATP binding cassette subfamily B member 1 Homo sapiens 116-130 34256125-1 2021 A series of eleven celastrol derivatives was designed, synthesized, and evaluated for their in vitro cytotoxic activities against six human cancer cell lines (A549, HepG2, HepAD38, PC3, DLD-1 Bax-Bak WT and DKO) and three human normal cells (LO2, BEAS-2B, CCD19Lu). celastrol 19-28 chromobox 8 Homo sapiens 181-184 34256125-1 2021 A series of eleven celastrol derivatives was designed, synthesized, and evaluated for their in vitro cytotoxic activities against six human cancer cell lines (A549, HepG2, HepAD38, PC3, DLD-1 Bax-Bak WT and DKO) and three human normal cells (LO2, BEAS-2B, CCD19Lu). celastrol 19-28 BCL2 associated X, apoptosis regulator Homo sapiens 192-195 34256125-1 2021 A series of eleven celastrol derivatives was designed, synthesized, and evaluated for their in vitro cytotoxic activities against six human cancer cell lines (A549, HepG2, HepAD38, PC3, DLD-1 Bax-Bak WT and DKO) and three human normal cells (LO2, BEAS-2B, CCD19Lu). celastrol 19-28 BCL2 antagonist/killer 1 Homo sapiens 196-199 34732120-0 2022 Celastrol inhibits the proliferation and induces apoptosis of colorectal cancer cells via downregulating NF-kappaB/COX-2 signaling pathways. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 105-114 34732120-0 2022 Celastrol inhibits the proliferation and induces apoptosis of colorectal cancer cells via downregulating NF-kappaB/COX-2 signaling pathways. celastrol 0-9 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-120 34732120-8 2022 RESULTS: Celastrol effectively inhibited CRC cell proliferation by activating caspase-dependent cell apoptosis and facilitating G1 cell cycle arrest in a dose-dependent manner, as well as cell migration and invasion by downregulating the MMP2 and MMP9. celastrol 9-18 matrix metallopeptidase 2 Homo sapiens 238-242 34732120-8 2022 RESULTS: Celastrol effectively inhibited CRC cell proliferation by activating caspase-dependent cell apoptosis and facilitating G1 cell cycle arrest in a dose-dependent manner, as well as cell migration and invasion by downregulating the MMP2 and MMP9. celastrol 9-18 matrix metallopeptidase 9 Homo sapiens 247-251 34732120-9 2022 Mechanistic protein expression revealed that celastrol suppressed the expression of COX-2 by inhibiting the phosphorylation of NF-kappaB p65 and subsequently leading to cytoplasmic retention of p65 protein, thereby inhibiting its nuclear translocation and transcription activities. celastrol 45-54 mitochondrially encoded cytochrome c oxidase II Homo sapiens 84-89 34732120-9 2022 Mechanistic protein expression revealed that celastrol suppressed the expression of COX-2 by inhibiting the phosphorylation of NF-kappaB p65 and subsequently leading to cytoplasmic retention of p65 protein, thereby inhibiting its nuclear translocation and transcription activities. celastrol 45-54 RELA proto-oncogene, NF-kB subunit Homo sapiens 127-140 34732120-9 2022 Mechanistic protein expression revealed that celastrol suppressed the expression of COX-2 by inhibiting the phosphorylation of NF-kappaB p65 and subsequently leading to cytoplasmic retention of p65 protein, thereby inhibiting its nuclear translocation and transcription activities. celastrol 45-54 RELA proto-oncogene, NF-kB subunit Homo sapiens 194-197 34732120-10 2022 CONCLUSION: These findings indicate that celastrol is an effective inhibitor for CRC, regulating the NF-kappaB/COX-2 pathway, leading to the inhibition of cell proliferation characterized by cell cycle arrest and caspase-dependent apoptosis, providing a potential alternative therapeutic agent for CRC patients. celastrol 41-50 nuclear factor kappa B subunit 1 Homo sapiens 101-110 34732120-10 2022 CONCLUSION: These findings indicate that celastrol is an effective inhibitor for CRC, regulating the NF-kappaB/COX-2 pathway, leading to the inhibition of cell proliferation characterized by cell cycle arrest and caspase-dependent apoptosis, providing a potential alternative therapeutic agent for CRC patients. celastrol 41-50 mitochondrially encoded cytochrome c oxidase II Homo sapiens 111-116 34702273-5 2021 Both in vitro and in vivo results demonstrated that celastrol inhibited the recruitment of M1 macrophage and the expression of TLR4 in corneal allografts through the TLR4/MyD88/NF-kappaB pathway, thereby significantly decreasing secretion of multiple pro-inflammatory cytokines to promote corneal allograft survival. celastrol 52-61 toll like receptor 4 Homo sapiens 127-131 34702273-5 2021 Both in vitro and in vivo results demonstrated that celastrol inhibited the recruitment of M1 macrophage and the expression of TLR4 in corneal allografts through the TLR4/MyD88/NF-kappaB pathway, thereby significantly decreasing secretion of multiple pro-inflammatory cytokines to promote corneal allograft survival. celastrol 52-61 toll like receptor 4 Homo sapiens 166-170 34702273-5 2021 Both in vitro and in vivo results demonstrated that celastrol inhibited the recruitment of M1 macrophage and the expression of TLR4 in corneal allografts through the TLR4/MyD88/NF-kappaB pathway, thereby significantly decreasing secretion of multiple pro-inflammatory cytokines to promote corneal allograft survival. celastrol 52-61 MYD88 innate immune signal transduction adaptor Homo sapiens 171-176 34702273-5 2021 Both in vitro and in vivo results demonstrated that celastrol inhibited the recruitment of M1 macrophage and the expression of TLR4 in corneal allografts through the TLR4/MyD88/NF-kappaB pathway, thereby significantly decreasing secretion of multiple pro-inflammatory cytokines to promote corneal allograft survival. celastrol 52-61 nuclear factor kappa B subunit 1 Homo sapiens 177-186 34720529-5 2021 Several studies show that drugs targeting Sp downregulation or NR4A1 antagonists are highly effective inhibitors of Sp/NR4A1-regulated pathways and genes in pancreatic and other cancer cells, and the triterpenoid celastrol is a novel dual-acting agent that targets both Sp TFs and NR4A1. celastrol 213-222 nuclear receptor subfamily 4 group A member 1 Homo sapiens 63-68 34720529-5 2021 Several studies show that drugs targeting Sp downregulation or NR4A1 antagonists are highly effective inhibitors of Sp/NR4A1-regulated pathways and genes in pancreatic and other cancer cells, and the triterpenoid celastrol is a novel dual-acting agent that targets both Sp TFs and NR4A1. celastrol 213-222 nuclear receptor subfamily 4 group A member 1 Homo sapiens 119-124 34720529-5 2021 Several studies show that drugs targeting Sp downregulation or NR4A1 antagonists are highly effective inhibitors of Sp/NR4A1-regulated pathways and genes in pancreatic and other cancer cells, and the triterpenoid celastrol is a novel dual-acting agent that targets both Sp TFs and NR4A1. celastrol 213-222 nuclear receptor subfamily 4 group A member 1 Homo sapiens 281-286 34579526-4 2021 The antitumor drug celastrol (CLT) and the photosensitizer indocyanine green (ICG) are then loaded in it to form CIPP. celastrol 19-28 PATJ, crumbs cell polarity complex component Mus musculus 113-117 34579526-4 2021 The antitumor drug celastrol (CLT) and the photosensitizer indocyanine green (ICG) are then loaded in it to form CIPP. celastrol 30-33 PATJ, crumbs cell polarity complex component Mus musculus 113-117 34796173-6 2021 In addition, we identified a small molecule compound Celastrol as an APE2 inhibitor that specifically compromises the binding of APE2 but not RPA to ssDNA and 3"-5" exonuclease activity of APE2 but not APE1. celastrol 53-62 apurinic/apyrimidinic endodeoxyribonuclease 2 Homo sapiens 69-73 34796173-6 2021 In addition, we identified a small molecule compound Celastrol as an APE2 inhibitor that specifically compromises the binding of APE2 but not RPA to ssDNA and 3"-5" exonuclease activity of APE2 but not APE1. celastrol 53-62 apurinic/apyrimidinic endodeoxyribonuclease 2 Homo sapiens 129-133 34796173-6 2021 In addition, we identified a small molecule compound Celastrol as an APE2 inhibitor that specifically compromises the binding of APE2 but not RPA to ssDNA and 3"-5" exonuclease activity of APE2 but not APE1. celastrol 53-62 apurinic/apyrimidinic endodeoxyribonuclease 2 Homo sapiens 189-193 34796173-7 2021 The impairment of ATR-Chk1 DDR pathway by Celastrol in Xenopus egg extracts and human pancreatic cancer cells highlights the physiological significance of Celastrol in the regulation of APE2 functionalities in genome integrity. celastrol 42-51 ATR serine/threonine kinase L homeolog Xenopus laevis 18-21 34796173-7 2021 The impairment of ATR-Chk1 DDR pathway by Celastrol in Xenopus egg extracts and human pancreatic cancer cells highlights the physiological significance of Celastrol in the regulation of APE2 functionalities in genome integrity. celastrol 42-51 checkpoint kinase 1 S homeolog Xenopus laevis 22-26 34796173-7 2021 The impairment of ATR-Chk1 DDR pathway by Celastrol in Xenopus egg extracts and human pancreatic cancer cells highlights the physiological significance of Celastrol in the regulation of APE2 functionalities in genome integrity. celastrol 42-51 apurinic/apyrimidinic endodeoxyribonuclease 2 Homo sapiens 186-190 34796173-7 2021 The impairment of ATR-Chk1 DDR pathway by Celastrol in Xenopus egg extracts and human pancreatic cancer cells highlights the physiological significance of Celastrol in the regulation of APE2 functionalities in genome integrity. celastrol 155-164 apurinic/apyrimidinic endodeoxyribonuclease 2 Homo sapiens 186-190 34600334-0 2021 The Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of Celastrol in Parkinson"s disease. celastrol 70-79 nuclear factor, erythroid derived 2, like 2 Mus musculus 4-8 34600334-0 2021 The Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of Celastrol in Parkinson"s disease. celastrol 70-79 NLR family, pyrin domain containing 3 Mus musculus 9-14 34600334-0 2021 The Nrf2-NLRP3-caspase-1 axis mediates the neuroprotective effects of Celastrol in Parkinson"s disease. celastrol 70-79 caspase 1 Mus musculus 15-24 34600334-4 2021 Here we show that celastrol protects against dopamine neuron loss, mitigates neuroinflammation, and relieves motor deficits in MPTP-induced PD mouse model and AAV-mediated human alpha-synuclein overexpression PD model. celastrol 18-27 synuclein alpha Homo sapiens 178-193 34600334-5 2021 Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD. celastrol 139-148 NFE2 like bZIP transcription factor 2 Homo sapiens 52-56 34600334-5 2021 Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD. celastrol 139-148 NLR family pyrin domain containing 3 Homo sapiens 58-63 34600334-5 2021 Whole-genome deep sequencing analysis revealed that Nrf2, NLRP3 and caspase-1 in SNc may be associated with the neuroprotective actions of celastrol in PD. celastrol 139-148 caspase 1 Homo sapiens 68-77 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 nuclear factor, erythroid derived 2, like 2 Mus musculus 45-49 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 NLR family, pyrin domain containing 3 Mus musculus 54-59 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 caspase 1 Mus musculus 67-76 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 NLR family, pyrin domain containing 3 Mus musculus 120-125 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 nuclear factor, erythroid derived 2, like 2 Mus musculus 227-231 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 NLR family, pyrin domain containing 3 Mus musculus 232-237 34600334-6 2021 By using multiple genetically modified mice (Nrf2-KO, NLRP3-KO and Caspase-1-KO), we identified that celastrol inhibits NLRP3 inflammasome activation, relieves motor deficits and nigrostriatal dopaminergic degeneration through Nrf2-NLRP3-caspase-1 pathway. celastrol 101-110 caspase 1 Mus musculus 238-247 34600334-7 2021 Taken together, these findings suggest that Nrf2-NLRP3-caspase-1 axis may serve as a key target of celastrol in PD treatment, and highlight the favorable properties of celastrol for neuroprotection, making celastrol as a promising disease-modifying agent for PD. celastrol 99-108 nuclear factor, erythroid derived 2, like 2 Mus musculus 44-48 34600334-7 2021 Taken together, these findings suggest that Nrf2-NLRP3-caspase-1 axis may serve as a key target of celastrol in PD treatment, and highlight the favorable properties of celastrol for neuroprotection, making celastrol as a promising disease-modifying agent for PD. celastrol 99-108 NLR family, pyrin domain containing 3 Mus musculus 49-54 34600334-7 2021 Taken together, these findings suggest that Nrf2-NLRP3-caspase-1 axis may serve as a key target of celastrol in PD treatment, and highlight the favorable properties of celastrol for neuroprotection, making celastrol as a promising disease-modifying agent for PD. celastrol 99-108 caspase 1 Mus musculus 55-64 34676604-0 2022 Celastrol attenuates high-fructose diet-induced inflammation and insulin resistance via inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity in rat adipose tissues. celastrol 0-9 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 102-144 34676604-4 2022 Herein, the present study was aimed to elucidate the mechanistic targets of celastrol co-administrations upon HFrD in rats and evaluate its potential to modulate 11beta-HSD1 activity. celastrol 76-85 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 162-173 34676604-6 2022 In rat adipose tissues, celastrol attenuated nuclear factor-kappa B (NF-kappaB)-driven inflammation, reduced c-Jun N-terminal kinases (JNK) phosphorylation, and mitigated oxidative stress via upregulated genes expression involved in mitochondrial biogenesis. celastrol 24-33 mitogen-activated protein kinase 8 Rattus norvegicus 109-133 34676604-6 2022 In rat adipose tissues, celastrol attenuated nuclear factor-kappa B (NF-kappaB)-driven inflammation, reduced c-Jun N-terminal kinases (JNK) phosphorylation, and mitigated oxidative stress via upregulated genes expression involved in mitochondrial biogenesis. celastrol 24-33 mitogen-activated protein kinase 8 Rattus norvegicus 135-138 34676604-8 2022 Celastrol exhibited a potent, selective and specific inhibitor of intracellular 11beta-HSD1 towards oxidoreductase activity (IC50 value = 4.3 nM) in comparison to other HSD-related enzymes. celastrol 0-9 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 80-91 34676604-10 2022 In conclusion, our results underscore the most likely conceivable mechanisms exhibited by celastrol against HFrD-induced metabolic dysregulations mainly through attenuating inflammation and insulin resistance, at least via specific inhibitions on 11beta-HSD1 activity in adipose tissues. celastrol 90-99 hydroxysteroid 11-beta dehydrogenase 1 Rattus norvegicus 247-258 34645818-0 2021 Phase separation of Nur77 mediates celastrol-induced mitophagy by promoting the liquidity of p62/SQSTM1 condensates. celastrol 35-44 nuclear receptor subfamily 4 group A member 1 Homo sapiens 20-25 34645818-0 2021 Phase separation of Nur77 mediates celastrol-induced mitophagy by promoting the liquidity of p62/SQSTM1 condensates. celastrol 35-44 sequestosome 1 Homo sapiens 93-96 34645818-0 2021 Phase separation of Nur77 mediates celastrol-induced mitophagy by promoting the liquidity of p62/SQSTM1 condensates. celastrol 35-44 sequestosome 1 Homo sapiens 97-103 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 nuclear receptor subfamily 4 group A member 1 Homo sapiens 47-52 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 nuclear receptor subfamily 4 group A member 1 Homo sapiens 66-69 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 nuclear receptor subfamily 4 group A member 1 Homo sapiens 71-77 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 nuclear receptor subfamily 4 group A member 1 Homo sapiens 82-87 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 sequestosome 1 Homo sapiens 199-202 34645818-3 2021 We previously discovered that nuclear receptor Nur77 (also called TR3, NGFI-B, or NR4A1) translocates from the nucleus to mitochondria to mediate celastrol-induced mitophagy through interaction with p62/SQSTM1. celastrol 146-155 sequestosome 1 Homo sapiens 203-209 34147915-0 2021 Celastrol inhibits rheumatoid arthritis through the ROS-NF-kappaB-NLRP3 inflammasome axis. celastrol 0-9 nuclear factor kappa B subunit 1 Homo sapiens 56-65 34549728-0 2021 PERK in POMC neurons connects celastrol with metabolism. celastrol 30-39 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 0-4 34549728-0 2021 PERK in POMC neurons connects celastrol with metabolism. celastrol 30-39 pro-opiomelanocortin-alpha Mus musculus 8-12 34549728-6 2021 The plant-based inhibitor of PERK, celastrol, increases leptin sensitivity, resulting in decreased food intake and body weight in a murine model of diet-induced obesity (DIO). celastrol 35-44 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 29-33 34549728-6 2021 The plant-based inhibitor of PERK, celastrol, increases leptin sensitivity, resulting in decreased food intake and body weight in a murine model of diet-induced obesity (DIO). celastrol 35-44 leptin Mus musculus 56-62 34549728-7 2021 Our data extend these observations by demonstrating that celastrol-induced improvements in leptin sensitivity and energy balance were attenuated in mice with PERK deficiency in POMC neurons. celastrol 57-66 leptin Mus musculus 91-97 34549728-7 2021 Our data extend these observations by demonstrating that celastrol-induced improvements in leptin sensitivity and energy balance were attenuated in mice with PERK deficiency in POMC neurons. celastrol 57-66 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 158-162 34549728-7 2021 Our data extend these observations by demonstrating that celastrol-induced improvements in leptin sensitivity and energy balance were attenuated in mice with PERK deficiency in POMC neurons. celastrol 57-66 pro-opiomelanocortin-alpha Mus musculus 177-181 34528509-4 2021 Importantly, brain treatment with celastrol, a pentacyclic triterpenoid, excites Oxt neurons and inhibits CAC progression, and this anti-tumor effect was significantly attenuated in Oxt neuron-lesioned mice. celastrol 34-43 oxytocin Mus musculus 81-84 34528509-4 2021 Importantly, brain treatment with celastrol, a pentacyclic triterpenoid, excites Oxt neurons and inhibits CAC progression, and this anti-tumor effect was significantly attenuated in Oxt neuron-lesioned mice. celastrol 34-43 oxytocin Mus musculus 182-185 34528509-5 2021 Furthermore, brain treatment with celastrol suppresses sympathetic neuronal activity in the celiac-superior mesenteric ganglion (CG-SMG), and activation of beta2 adrenergic receptor abolishes the anti-tumor effect of Oxt neuron activation or centrally administered celastrol. celastrol 265-274 adrenergic receptor, beta 2 Mus musculus 156-181 34147915-0 2021 Celastrol inhibits rheumatoid arthritis through the ROS-NF-kappaB-NLRP3 inflammasome axis. celastrol 0-9 NLR family pyrin domain containing 3 Homo sapiens 66-71 34147915-6 2021 The secretion of interleukin (IL)-1beta and IL-18 in the serum of CFA-induced rats and supernatants of THP-1 cells exposed to Cel was significantly decreased. celastrol 126-129 interleukin 1 alpha Rattus norvegicus 17-39 34147915-6 2021 The secretion of interleukin (IL)-1beta and IL-18 in the serum of CFA-induced rats and supernatants of THP-1 cells exposed to Cel was significantly decreased. celastrol 126-129 interleukin 18 Rattus norvegicus 44-49 34526895-0 2021 Creation of an Anti-Inflammatory, Leptin-Dependent Anti-Obesity Celastrol Mimic with Better Druggability. celastrol 64-73 leptin Mus musculus 34-40 34174395-8 2021 Interestingly, Cel treatment increased the mRNA and protein levels of heme oxygenase-1 (HMOX-1), and reduced the levels of reactive oxygen species (ROS) in VSMCs. celastrol 15-18 heme oxygenase 1 Rattus norvegicus 88-94 34250995-7 2021 For this purpose, we constructed a hybrid nanoplatform by fusing CLT (Celastrol)-Loaded PEGylated lipids with the DC2.4 cell membrane (M-LIP-CLT) to achieve targeted treatment of Kras-mutant pancreatic cancer. celastrol 70-79 Kirsten rat sarcoma viral oncogene homolog Mus musculus 179-183 34372857-0 2021 Celastrol exerts a neuroprotective effect by directly binding to HMGB1 protein in cerebral ischemia-reperfusion. celastrol 0-9 high mobility group box 1 Rattus norvegicus 65-70 34174395-0 2021 Up-regulation of heme oxygenase-1 by celastrol alleviates oxidative stress and vascular calcification in chronic kidney disease. celastrol 37-46 heme oxygenase 1 Rattus norvegicus 17-33 34174395-8 2021 Interestingly, Cel treatment increased the mRNA and protein levels of heme oxygenase-1 (HMOX-1), and reduced the levels of reactive oxygen species (ROS) in VSMCs. celastrol 15-18 heme oxygenase 1 Rattus norvegicus 70-86 34174395-9 2021 Furthermore, both pharmacological inhibition of HMOX-1 and knockdown of HMOX-1 by siRNA independently counteracted the inhibitory effect of Cel on vascular calcification. celastrol 140-143 heme oxygenase 1 Rattus norvegicus 48-54 34174395-9 2021 Furthermore, both pharmacological inhibition of HMOX-1 and knockdown of HMOX-1 by siRNA independently counteracted the inhibitory effect of Cel on vascular calcification. celastrol 140-143 heme oxygenase 1 Rattus norvegicus 72-78 34174395-12 2021 Collectively, our results suggest that up-regulation of HMOX-1 is required for the inhibitory effect of Cel on vascular calcification. celastrol 104-107 heme oxygenase 1 Mus musculus 56-62 34490381-7 2021 This literature review therefore focuses on Celastrol"s anti-inflammatory and antioxidant activities, alongside its other potential therapeutic activities, and its ability to impede the pathways that are thought to be involved in the development of HFpEF, such as the JAK2/STAT pathway, to elucidate the potential therapeutic role of this bioactive compound, in the treatment of HFpEF. celastrol 44-53 Janus kinase 2 Homo sapiens 268-272 34170694-2 2021 Celastrol, a natural friedelane triterpenoid, can disrupt the Hsp90-Cdc37 interaction to provide antitumor effects. celastrol 0-9 heat shock protein 90 alpha family class A member 1 Homo sapiens 62-67 34325521-7 2021 Consistent with genetic manipulation, pharmacological activation of Nur77 by celastrol showed beneficial effects against AAA. celastrol 77-86 nuclear receptor subfamily 4, group A, member 1 Mus musculus 68-73 34367293-8 2021 Celastrol-treated cells increased quantities of proangiogenic cytokines compared to vehicle-pretreated cells, with a significant 3.0-fold and 1.8-fold increase of VEGFa and SDF-1alpha, respectively (p < 0.05). celastrol 0-9 vascular endothelial growth factor A Rattus norvegicus 163-168 34170694-2 2021 Celastrol, a natural friedelane triterpenoid, can disrupt the Hsp90-Cdc37 interaction to provide antitumor effects. celastrol 0-9 cell division cycle 37, HSP90 cochaperone Homo sapiens 68-73 34170694-3 2021 In this study, 31 new celastrol derivatives, 2a-2d, 3a-3g, and 4a-4t, were designed and synthesized, and their Hsp90-Cdc37 disruption activities and antiproliferative activities against cancer cells were evaluated. celastrol 22-31 heat shock protein 90 alpha family class A member 1 Homo sapiens 111-116 34170694-3 2021 In this study, 31 new celastrol derivatives, 2a-2d, 3a-3g, and 4a-4t, were designed and synthesized, and their Hsp90-Cdc37 disruption activities and antiproliferative activities against cancer cells were evaluated. celastrol 22-31 cell division cycle 37, HSP90 cochaperone Homo sapiens 117-122 34305512-0 2021 Corrigendum: Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-kappaB Signaling Pathway. celastrol 40-49 high mobility group box 1 Rattus norvegicus 108-113 34337076-6 2021 The results from Annexin V/PI staining and flow cytometry analysis suggested that celastrol enhanced tamoxifen-mediated apoptosis. celastrol 82-91 annexin A5 Homo sapiens 17-26 34337076-8 2021 Moreover, the distribution of LC3 was monitored by immunofluorescence, and the changes in the LC3II and P62 levels detected by western blot analysis suggested that celastrol in combination with tamoxifen triggered autophagy. celastrol 164-173 microtubule associated protein 1 light chain 3 alpha Homo sapiens 30-33 34337076-10 2021 However, in an MCF-7-implanted nude mouse model, it was possible to detect significantly decreased tumour volumes and tumour weights and decreased p-Akt and p-mTOR protein expression in the celastrol+tamoxifen group. celastrol 190-199 thymoma viral proto-oncogene 1 Mus musculus 149-152 34337076-10 2021 However, in an MCF-7-implanted nude mouse model, it was possible to detect significantly decreased tumour volumes and tumour weights and decreased p-Akt and p-mTOR protein expression in the celastrol+tamoxifen group. celastrol 190-199 mechanistic target of rapamycin kinase Mus musculus 159-163 34285658-10 2021 Further, the inhibitory effect of LPS on a minimal SLC23A2 promoter was attenuated when either the binding site for the transcription factor Sp1 was mutated or cells were treated with the NF-kappaB inhibitor, celastrol. celastrol 209-218 solute carrier family 23 member 2 Homo sapiens 51-58 34285658-10 2021 Further, the inhibitory effect of LPS on a minimal SLC23A2 promoter was attenuated when either the binding site for the transcription factor Sp1 was mutated or cells were treated with the NF-kappaB inhibitor, celastrol. celastrol 209-218 nuclear factor kappa B subunit 1 Homo sapiens 188-197 34182541-9 2021 Celastrol protected blood-brain bairrer integrity through inhibiting MMP-9 expression and anti-neuroinflammatory effects. celastrol 0-9 matrix metallopeptidase 9 Rattus norvegicus 69-74 34182541-10 2021 Additionally, necroptosis-related proteins RIP3 and MLKL were down-regulated and PI-positive cells in the basal cortex were less in the celastrol-treated SAH group than that in untreated SAH group. celastrol 136-145 myosin phosphatase Rho interacting protein Rattus norvegicus 43-47 34182541-10 2021 Additionally, necroptosis-related proteins RIP3 and MLKL were down-regulated and PI-positive cells in the basal cortex were less in the celastrol-treated SAH group than that in untreated SAH group. celastrol 136-145 mixed lineage kinase domain like pseudokinase Rattus norvegicus 52-56 34194230-0 2021 Celastrol Modulates Multiple Signaling Pathways to Inhibit Proliferation of Pancreatic Cancer via DDIT3 and ATF3 Up-Regulation and RRM2 and MCM4 Down-Regulation. celastrol 0-9 DNA damage inducible transcript 3 Homo sapiens 98-103 34194230-0 2021 Celastrol Modulates Multiple Signaling Pathways to Inhibit Proliferation of Pancreatic Cancer via DDIT3 and ATF3 Up-Regulation and RRM2 and MCM4 Down-Regulation. celastrol 0-9 activating transcription factor 3 Homo sapiens 108-112 34194230-0 2021 Celastrol Modulates Multiple Signaling Pathways to Inhibit Proliferation of Pancreatic Cancer via DDIT3 and ATF3 Up-Regulation and RRM2 and MCM4 Down-Regulation. celastrol 0-9 ribonucleotide reductase regulatory subunit M2 Homo sapiens 131-135 34194230-0 2021 Celastrol Modulates Multiple Signaling Pathways to Inhibit Proliferation of Pancreatic Cancer via DDIT3 and ATF3 Up-Regulation and RRM2 and MCM4 Down-Regulation. celastrol 0-9 minichromosome maintenance complex component 4 Homo sapiens 140-144 34194230-9 2021 Celastrol modulated many signaling genes and its cytotoxic effect was mainly mediated via over-expression of ATF3 and DDIT3, and down-expression of RRM2 and MCM4. celastrol 0-9 activating transcription factor 3 Homo sapiens 109-113 34194230-9 2021 Celastrol modulated many signaling genes and its cytotoxic effect was mainly mediated via over-expression of ATF3 and DDIT3, and down-expression of RRM2 and MCM4. celastrol 0-9 DNA damage inducible transcript 3 Homo sapiens 118-123 34194230-9 2021 Celastrol modulated many signaling genes and its cytotoxic effect was mainly mediated via over-expression of ATF3 and DDIT3, and down-expression of RRM2 and MCM4. celastrol 0-9 ribonucleotide reductase regulatory subunit M2 Homo sapiens 148-152 34194230-9 2021 Celastrol modulated many signaling genes and its cytotoxic effect was mainly mediated via over-expression of ATF3 and DDIT3, and down-expression of RRM2 and MCM4. celastrol 0-9 minichromosome maintenance complex component 4 Homo sapiens 157-161 34982057-0 2021 Celastrol promotes chondrocyte autophagy by regulating mTOR expression. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 55-59 34326694-0 2021 Celastrol ameliorates vascular neointimal hyperplasia through Wnt5a-involved autophagy. celastrol 0-9 Wnt family member 5A Homo sapiens 62-67 34326694-6 2021 It was revealed that autophagy promoted by celastrol could induce the lysosomal degradation of c-MYC, which might be a possible mechanism contributing to the reduction of VSMCs proliferation. celastrol 43-52 MYC proto-oncogene, bHLH transcription factor Homo sapiens 95-100 34326694-7 2021 The Wnt5a/PKC/mTOR signaling pathway was found to be an underlying mechanism for celastrol to induce autophagy and inhibit the VSMCs proliferation. celastrol 81-90 Wnt family member 5A Homo sapiens 4-9 34326694-7 2021 The Wnt5a/PKC/mTOR signaling pathway was found to be an underlying mechanism for celastrol to induce autophagy and inhibit the VSMCs proliferation. celastrol 81-90 mechanistic target of rapamycin kinase Homo sapiens 14-18 34094828-7 2021 Taken together, our study identifies celastrol, which directly targets CAP1 in macrophages, might be a promising drug candidate for the treatment of inflammatory metabolic diseases, such as metabolic syndrome. celastrol 37-46 CAP, adenylate cyclase-associated protein 1 (yeast) Mus musculus 71-75 34149427-0 2021 Celastrol Attenuates RANKL-Induced Osteoclastogenesis in vitro and Reduces Titanium Particle-Induced Osteolysis and Ovariectomy-Induced Bone Loss in vivo. celastrol 0-9 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 21-26 34149427-5 2021 We demonstrated that celastrol inhibited the receptor activator of nuclear factor kappaB ligand-induced osteoclastogenesis and the bone resorptive function of osteoclasts in vitro by inhibiting the activation of transforming growth factor beta-activated kinase 1-mediated NF-kappaB and mitogen-activated protein kinase signaling pathways and downregulating osteoclastogenesis marker-related genes. celastrol 21-30 mitogen-activated protein kinase kinase kinase 7 Mus musculus 212-262 34149427-5 2021 We demonstrated that celastrol inhibited the receptor activator of nuclear factor kappaB ligand-induced osteoclastogenesis and the bone resorptive function of osteoclasts in vitro by inhibiting the activation of transforming growth factor beta-activated kinase 1-mediated NF-kappaB and mitogen-activated protein kinase signaling pathways and downregulating osteoclastogenesis marker-related genes. celastrol 21-30 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 272-281 34185400-0 2021 Celastrol alleviates comorbid obesity and depression by directly binding amygdala HnRNPA1 in a mouse model. celastrol 0-9 heterogeneous nuclear ribonucleoprotein A1 Mus musculus 82-89 34094828-0 2021 Celastrol targets adenylyl cyclase-associated protein 1 to reduce macrophages-mediated inflammation and ameliorates high fat diet-induced metabolic syndrome in mice. celastrol 0-9 CAP, adenylate cyclase-associated protein 1 (yeast) Mus musculus 18-55 34094828-3 2021 Here, we report celastrol, a traditional Chinese medicine, can improve high fat diet-induced metabolic syndrome through suppressing resistin-induced inflammation. celastrol 16-25 resistin Mus musculus 132-140 34094828-4 2021 Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-kappaB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. celastrol 17-26 CAP, adenylate cyclase-associated protein 1 (yeast) Mus musculus 36-73 34094828-4 2021 Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-kappaB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. celastrol 17-26 CAP, adenylate cyclase-associated protein 1 (yeast) Mus musculus 75-79 34094828-4 2021 Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-kappaB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. celastrol 17-26 CAP, adenylate cyclase-associated protein 1 (yeast) Mus musculus 118-122 34094828-4 2021 Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-kappaB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. celastrol 17-26 resistin Mus musculus 127-135 34094828-4 2021 Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)-protein kinase A (PKA)-nuclear factor kappa-B (NF-kappaB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. celastrol 17-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 242-251 34114395-0 2021 Celastrol induces caspase-dependent apoptosis of hepatocellular carcinoma cells by suppression of mammalian target of rapamycin. celastrol 0-9 caspase 8 Homo sapiens 18-25 34114395-0 2021 Celastrol induces caspase-dependent apoptosis of hepatocellular carcinoma cells by suppression of mammalian target of rapamycin. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 98-127 34114395-8 2021 Western blot assays indicated that celastrol up-regulated cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, and cleaved-PARP by inhibiting the phosphorylation of mTOR in HepG2 cells. celastrol 35-44 caspase 8 Homo sapiens 85-94 34114395-8 2021 Western blot assays indicated that celastrol up-regulated cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, and cleaved-PARP by inhibiting the phosphorylation of mTOR in HepG2 cells. celastrol 35-44 caspase 9 Homo sapiens 104-113 34114395-8 2021 Western blot assays indicated that celastrol up-regulated cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, and cleaved-PARP by inhibiting the phosphorylation of mTOR in HepG2 cells. celastrol 35-44 poly(ADP-ribose) polymerase 1 Homo sapiens 127-131 34114395-8 2021 Western blot assays indicated that celastrol up-regulated cleaved-caspase-3, cleaved-caspase-8, cleaved-caspase-9, and cleaved-PARP by inhibiting the phosphorylation of mTOR in HepG2 cells. celastrol 35-44 mechanistic target of rapamycin kinase Homo sapiens 169-173 34114395-10 2021 Celastrol also induced caspase-dependent apoptosis (up-regulation of cleaved-caspase- 3, -8, -9, and cleaved-PARP) and inhibited the activation of mTOR in vivo. celastrol 0-9 caspase 8 Homo sapiens 23-30 34114395-10 2021 Celastrol also induced caspase-dependent apoptosis (up-regulation of cleaved-caspase- 3, -8, -9, and cleaved-PARP) and inhibited the activation of mTOR in vivo. celastrol 0-9 poly(ADP-ribose) polymerase 1 Homo sapiens 109-113 34114395-10 2021 Celastrol also induced caspase-dependent apoptosis (up-regulation of cleaved-caspase- 3, -8, -9, and cleaved-PARP) and inhibited the activation of mTOR in vivo. celastrol 0-9 mechanistic target of rapamycin kinase Homo sapiens 147-151 34114395-11 2021 CONCLUSION: Celastrol induces caspase-dependent apoptosis in HCC cells by inhibiting the activation of mTOR. celastrol 12-21 caspase 8 Homo sapiens 30-37 34114395-11 2021 CONCLUSION: Celastrol induces caspase-dependent apoptosis in HCC cells by inhibiting the activation of mTOR. celastrol 12-21 mechanistic target of rapamycin kinase Homo sapiens 103-107 34072312-6 2021 Moreover, triterpenoids containing a lactone ring and/or quinone-like substructures, e.g., bruceantin, whitaferin A, withanolide F, celastrol, and pristimerin, displayed remarkable activity, with the latter two compounds acting as inhibitors of both NF-kappaB and proteasome chymotrypsin-like activity. celastrol 132-141 nuclear factor kappa B subunit 1 Homo sapiens 250-259 35576663-0 2022 Celastrol and thymoquinone alleviate aluminum chloride-induced neurotoxicity: Behavioral psychomotor performance, neurotransmitter level, oxidative-inflammatory markers, and BDNF expression in rat brain. celastrol 0-9 brain-derived neurotrophic factor Rattus norvegicus 174-178 34112289-9 2021 CONCLUSIONS: Celastrol may regulate the expression and release of inflammatory factors by inhibiting the TLR4/NF-kappaB pathway, thereby alleviating the ALI induced by sepsis in rats. celastrol 13-22 toll-like receptor 4 Rattus norvegicus 105-109 34428765-0 2021 Celastrol Exerts Cardioprotective Effect in Rheumatoid Arthritis by Inhibiting TLR2/HMGB1 Signaling Pathway-Mediated Autophagy. celastrol 0-9 toll-like receptor 2 Rattus norvegicus 79-83 34428765-0 2021 Celastrol Exerts Cardioprotective Effect in Rheumatoid Arthritis by Inhibiting TLR2/HMGB1 Signaling Pathway-Mediated Autophagy. celastrol 0-9 high mobility group box 1 Rattus norvegicus 84-89 34428765-10 2021 Compared with CIA model, Celastrol treatment could suppress the release of inflammatory cytokines, including TNF-alpha, IL-6, IL-1beta, as well as inhibiting the expressions of Bax, cleaved caspase3, collagen I, collagen III and alpha-SMA. celastrol 25-34 tumor necrosis factor Rattus norvegicus 109-118 34428765-10 2021 Compared with CIA model, Celastrol treatment could suppress the release of inflammatory cytokines, including TNF-alpha, IL-6, IL-1beta, as well as inhibiting the expressions of Bax, cleaved caspase3, collagen I, collagen III and alpha-SMA. celastrol 25-34 interleukin 6 Rattus norvegicus 120-124 34428765-10 2021 Compared with CIA model, Celastrol treatment could suppress the release of inflammatory cytokines, including TNF-alpha, IL-6, IL-1beta, as well as inhibiting the expressions of Bax, cleaved caspase3, collagen I, collagen III and alpha-SMA. celastrol 25-34 interleukin 1 alpha Rattus norvegicus 126-134 34428765-10 2021 Compared with CIA model, Celastrol treatment could suppress the release of inflammatory cytokines, including TNF-alpha, IL-6, IL-1beta, as well as inhibiting the expressions of Bax, cleaved caspase3, collagen I, collagen III and alpha-SMA. celastrol 25-34 BCL2 associated X, apoptosis regulator Rattus norvegicus 177-180 34428765-10 2021 Compared with CIA model, Celastrol treatment could suppress the release of inflammatory cytokines, including TNF-alpha, IL-6, IL-1beta, as well as inhibiting the expressions of Bax, cleaved caspase3, collagen I, collagen III and alpha-SMA. celastrol 25-34 caspase 3 Rattus norvegicus 190-198 34428765-11 2021 In addition to that, Celastrol treatment can attenuate cell apoptosis and fibrosis of cardiomyocytes and elevate Bcl-2 expression. celastrol 21-30 BCL2, apoptosis regulator Rattus norvegicus 113-118 34428765-12 2021 RA induced cell autophagy can be suppressed by Celastrol through inhibiting the activation of TLR2/HMGB1 signal pathway. celastrol 47-56 toll-like receptor 2 Rattus norvegicus 94-98 34428765-12 2021 RA induced cell autophagy can be suppressed by Celastrol through inhibiting the activation of TLR2/HMGB1 signal pathway. celastrol 47-56 high mobility group box 1 Rattus norvegicus 99-104 34428765-13 2021 CONCLUSION: Celastrol can regulate TLR2/HMGB1 signal pathway to suppress autophagy and therefore exert cardioprotective effect in RA. celastrol 12-21 toll-like receptor 2 Rattus norvegicus 35-39 34428765-13 2021 CONCLUSION: Celastrol can regulate TLR2/HMGB1 signal pathway to suppress autophagy and therefore exert cardioprotective effect in RA. celastrol 12-21 high mobility group box 1 Rattus norvegicus 40-45 34472389-0 2021 RETRACTION NOTICE: Tripterine up-regulates miR-223 to alleviate lipopolysaccharide-induced damage in murine chondrogenic ATDC5 cells. celastrol 19-29 microRNA 223 Mus musculus 43-50 35596191-0 2022 Celastrol mitigates inflammation in sepsis by inhibiting the PKM2-dependent Warburg effect. celastrol 0-9 pyruvate kinase, muscle Mus musculus 61-65 35605435-0 2022 Phytosomal tripterine with selenium modification attenuates the cytotoxicity and restrains the inflammatory evolution via inhibiting NLRP3 inflammasome activation and pyroptosis. celastrol 11-21 NLR family, pyrin domain containing 3 Mus musculus 133-138 35583119-3 2022 Celastrol (CST) was directly assembled into a discrete nanomedicine by precipitation, and then CST nanoparticles (CNPs) inhibited drug efflux pumps by activating HSF-1 expression and promoting HSF-1 translocation into nucleus to suppress the Pgp expression. celastrol 0-9 heat shock transcription factor 1 Homo sapiens 162-167 35583119-3 2022 Celastrol (CST) was directly assembled into a discrete nanomedicine by precipitation, and then CST nanoparticles (CNPs) inhibited drug efflux pumps by activating HSF-1 expression and promoting HSF-1 translocation into nucleus to suppress the Pgp expression. celastrol 0-9 heat shock transcription factor 1 Homo sapiens 193-198 35583119-3 2022 Celastrol (CST) was directly assembled into a discrete nanomedicine by precipitation, and then CST nanoparticles (CNPs) inhibited drug efflux pumps by activating HSF-1 expression and promoting HSF-1 translocation into nucleus to suppress the Pgp expression. celastrol 0-9 phosphoglycolate phosphatase Homo sapiens 242-245 35364220-2 2022 In this work, a biomimetic BBB-penetrating albumin nanosystem modified by a brain-targeting peptide was designed for co-delivering a TGF-beta receptor I (TGFbetaRI) inhibitor (LY2157299) and an mTOR inhibitor (celastrol). celastrol 210-219 mechanistic target of rapamycin kinase Mus musculus 194-198 35143937-8 2022 The hepatotoxicity induced by TP and Cel also inhibited PPARalpha and upregulated IL6-STAT3 axis, which could be alleviated following by PPARalpha activation. celastrol 37-40 peroxisome proliferator activated receptor alpha Mus musculus 56-65 35143937-8 2022 The hepatotoxicity induced by TP and Cel also inhibited PPARalpha and upregulated IL6-STAT3 axis, which could be alleviated following by PPARalpha activation. celastrol 37-40 peroxisome proliferator activated receptor alpha Mus musculus 137-146 35478244-0 2022 Celastrol suppresses the growth of vestibular schwannoma in mice by promoting the degradation of beta-catenin. celastrol 0-9 catenin (cadherin associated protein), beta 1 Mus musculus 97-109 35478244-8 2022 In HEI-193 and SC4 cells, we demonstrated that celastrol (0.1, 0.5 muM) dose-dependently inhibited TOPFlash reporter activity and protein expression of beta-catenin, but not mRNA level of beta-catenin. celastrol 47-56 catenin beta 1 Homo sapiens 188-200 35478244-9 2022 Furthermore, celastrol accelerated the degradation of beta-catenin by promoting the formation of the beta-catenin destruction complex. celastrol 13-22 catenin beta 1 Homo sapiens 54-66 35478244-8 2022 In HEI-193 and SC4 cells, we demonstrated that celastrol (0.1, 0.5 muM) dose-dependently inhibited TOPFlash reporter activity and protein expression of beta-catenin, but not mRNA level of beta-catenin. celastrol 47-56 catenin beta 1 Homo sapiens 152-164 35478244-9 2022 Furthermore, celastrol accelerated the degradation of beta-catenin by promoting the formation of the beta-catenin destruction complex. celastrol 13-22 catenin beta 1 Homo sapiens 101-113 35478244-12 2022 Collectively, this study demonstrates that celastrol can inhibit Wnt/beta-catenin signaling by promoting the degradation of beta-catenin, consequently inhibiting the growth of VS. celastrol 43-52 catenin (cadherin associated protein), beta 1 Mus musculus 69-81 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 nitric oxide synthase 2 Homo sapiens 152-183 35478244-12 2022 Collectively, this study demonstrates that celastrol can inhibit Wnt/beta-catenin signaling by promoting the degradation of beta-catenin, consequently inhibiting the growth of VS. celastrol 43-52 catenin (cadherin associated protein), beta 1 Mus musculus 124-136 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 nitric oxide synthase 2 Homo sapiens 185-189 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 192-208 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 210-214 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 tumor necrosis factor Homo sapiens 217-244 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 tumor necrosis factor Homo sapiens 246-255 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 C-C motif chemokine ligand 2 Homo sapiens 270-275 35530963-9 2022 Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-alpha), chemokines (CCL-2, and CXCL-10), as well as chemokines. celastrol 20-29 C-X-C motif chemokine ligand 10 Homo sapiens 281-288 35530963-10 2022 And Celastrol could regulate mitochondrial fission and fusion by promoting the phosphorylation of the Drp1 at the Ser637 site, thereby inhibiting mitochondrial fission. celastrol 4-13 dynamin 1 like Homo sapiens 102-106 35530963-11 2022 At the same time, by up-regulating the level of the Mfn2, Celastrol also promoted mitochondrial fusion. celastrol 58-67 mitofusin 2 Homo sapiens 52-56 35530963-13 2022 We also explored the relationship between Celastrol and the nuclear receptor Nur77 and found that it could up-regulate the expression of Nur77. celastrol 42-51 nuclear receptor subfamily 4 group A member 1 Homo sapiens 77-82 35530963-13 2022 We also explored the relationship between Celastrol and the nuclear receptor Nur77 and found that it could up-regulate the expression of Nur77. celastrol 42-51 nuclear receptor subfamily 4 group A member 1 Homo sapiens 137-142 35530963-14 2022 Conclusions: Our study found that Celastrol could reduce inflammation by regulating Drp1 dependent mitochondrial fission and fusion, as well as the ERK1/2, p38, NF-kappaB signaling pathways. celastrol 34-43 dynamin 1 like Homo sapiens 84-88 35530963-14 2022 Conclusions: Our study found that Celastrol could reduce inflammation by regulating Drp1 dependent mitochondrial fission and fusion, as well as the ERK1/2, p38, NF-kappaB signaling pathways. celastrol 34-43 mitogen-activated protein kinase 3 Homo sapiens 148-154 35530963-14 2022 Conclusions: Our study found that Celastrol could reduce inflammation by regulating Drp1 dependent mitochondrial fission and fusion, as well as the ERK1/2, p38, NF-kappaB signaling pathways. celastrol 34-43 mitogen-activated protein kinase 1 Homo sapiens 156-159 35530963-14 2022 Conclusions: Our study found that Celastrol could reduce inflammation by regulating Drp1 dependent mitochondrial fission and fusion, as well as the ERK1/2, p38, NF-kappaB signaling pathways. celastrol 34-43 nuclear factor kappa B subunit 1 Homo sapiens 161-170 35107368-3 2022 Iinhibition of the Hsp90/Cdc37 complex by inhibitors (17-AAG and celastrol) or shRNAs significantly reduced expression levels of viral proteins and virus yield, suggesting that the Hsp90/Cdc37 chaperone complex functions in virus replication. celastrol 65-74 heat shock protein 90 alpha family class A member 1 Homo sapiens 19-24 35419676-0 2022 Celastrol Induces Apoptosis and Autophagy via the AKT/mTOR Signaling Pathway in the Pituitary ACTH-secreting Adenoma Cells. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 50-53 35419676-0 2022 Celastrol Induces Apoptosis and Autophagy via the AKT/mTOR Signaling Pathway in the Pituitary ACTH-secreting Adenoma Cells. celastrol 0-9 mechanistic target of rapamycin kinase Mus musculus 54-58 35419676-0 2022 Celastrol Induces Apoptosis and Autophagy via the AKT/mTOR Signaling Pathway in the Pituitary ACTH-secreting Adenoma Cells. celastrol 0-9 pro-opiomelanocortin-alpha Mus musculus 94-98 35419676-2 2022 Previous studies have shown that celastrol has antitumor effects on a variety of tumor cells via the AKT/mTOR signaling. celastrol 33-42 thymoma viral proto-oncogene 1 Mus musculus 101-104 35419676-2 2022 Previous studies have shown that celastrol has antitumor effects on a variety of tumor cells via the AKT/mTOR signaling. celastrol 33-42 mechanistic target of rapamycin kinase Mus musculus 105-109 35419676-8 2022 Finally, the potential involvement of AKT/mTOR signaling in celastrol"s mechanism was assessed. celastrol 60-69 mechanistic target of rapamycin kinase Mus musculus 42-46 35419676-12 2022 CONCLUSION: Celastrol exerts potent antitumor effects on ACTH-secreting adenoma by downregulating the AKT/mTOR signaling in vitro and in vivo. celastrol 12-21 pro-opiomelanocortin-alpha Mus musculus 57-61 35419676-12 2022 CONCLUSION: Celastrol exerts potent antitumor effects on ACTH-secreting adenoma by downregulating the AKT/mTOR signaling in vitro and in vivo. celastrol 12-21 thymoma viral proto-oncogene 1 Mus musculus 102-105 35419676-12 2022 CONCLUSION: Celastrol exerts potent antitumor effects on ACTH-secreting adenoma by downregulating the AKT/mTOR signaling in vitro and in vivo. celastrol 12-21 mechanistic target of rapamycin kinase Mus musculus 106-110 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 12-21 heat shock protein 90 alpha family class A member 1 Homo sapiens 54-59 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 12-21 cell division cycle 37, HSP90 cochaperone Homo sapiens 60-65 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 23-26 heat shock protein 90 alpha family class A member 1 Homo sapiens 54-59 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 23-26 cell division cycle 37, HSP90 cochaperone Homo sapiens 60-65 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 183-186 heat shock protein 90 alpha family class A member 1 Homo sapiens 54-59 35238566-1 2022 To discover celastrol (CEL) derivatives with enhanced Hsp90-Cdc37 inhibition, C-20-COOH was introduced with various substituted imidazoles, which might affect the Michael addition of CEL by nucleophilic attack. celastrol 183-186 cell division cycle 37, HSP90 cochaperone Homo sapiens 60-65 35302751-0 2022 Integrated Mass Spectrometry Reveals Celastrol As a Novel Catechol-O-methyltransferase Inhibitor. celastrol 37-46 catechol-O-methyltransferase Homo sapiens 58-86 35107368-3 2022 Iinhibition of the Hsp90/Cdc37 complex by inhibitors (17-AAG and celastrol) or shRNAs significantly reduced expression levels of viral proteins and virus yield, suggesting that the Hsp90/Cdc37 chaperone complex functions in virus replication. celastrol 65-74 cell division cycle 37, HSP90 cochaperone Homo sapiens 25-30 35051865-12 2022 In IMQ-induced psoriatic dermatitis, Cel gel reduced the secretion of interleukin (IL)- 23 by Langerhans cells, suppressed the interaction between Langerhans cells and gammadeltaT cells, and decreased the number of activated gammadeltaT cells and related IL-17 secretion, alleviating psoriasis-like inflammation. celastrol 37-40 interleukin 23, alpha subunit p19 Mus musculus 70-90 35302751-2 2022 Here, we used multiple mass-spectrometry-based approaches to identify catechol-O-methyltransferase (COMT) as a major binding target of celastrol and characterized their interaction comprehensively. celastrol 135-144 catechol-O-methyltransferase Homo sapiens 70-98 35302751-2 2022 Here, we used multiple mass-spectrometry-based approaches to identify catechol-O-methyltransferase (COMT) as a major binding target of celastrol and characterized their interaction comprehensively. celastrol 135-144 catechol-O-methyltransferase Homo sapiens 100-104 35302751-3 2022 Celastrol was found to inhibit the enzymatic activity of COMT and increased the dopamine level in neuroendocrine chromaffin cells significantly. celastrol 0-9 catechol-O-methyltransferase Homo sapiens 57-61 35302751-4 2022 Our study not only revealed a novel binding target of celastrol but also provided a new scaffold and cysteine hot spot for developing new generation COMT inhibitors in combating neurological disorders. celastrol 54-63 catechol-O-methyltransferase Homo sapiens 149-153 35359864-0 2022 Celastrol Alleviates Autoimmune Hepatitis Through the PI3K/AKT Signaling Pathway Based on Network Pharmacology and Experiments. celastrol 0-9 thymoma viral proto-oncogene 1 Mus musculus 59-62 35359864-7 2022 Among them, PIK3R1, SRC, MAPK1, AKT1, and HRAS were selected as the top 5 closely related targets to celastrol. celastrol 101-110 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 12-18 35359864-7 2022 Among them, PIK3R1, SRC, MAPK1, AKT1, and HRAS were selected as the top 5 closely related targets to celastrol. celastrol 101-110 Rous sarcoma oncogene Mus musculus 20-23 35359864-7 2022 Among them, PIK3R1, SRC, MAPK1, AKT1, and HRAS were selected as the top 5 closely related targets to celastrol. celastrol 101-110 mitogen-activated protein kinase 1 Mus musculus 25-30 35359864-7 2022 Among them, PIK3R1, SRC, MAPK1, AKT1, and HRAS were selected as the top 5 closely related targets to celastrol. celastrol 101-110 thymoma viral proto-oncogene 1 Mus musculus 32-36 35359864-7 2022 Among them, PIK3R1, SRC, MAPK1, AKT1, and HRAS were selected as the top 5 closely related targets to celastrol. celastrol 101-110 Harvey rat sarcoma virus oncogene Mus musculus 42-46 35359864-9 2022 Subsequently, celastrol administration significantly ameliorated hepatitis and liver fibrosis by reducing AKT1 and PI3K phosphorylation in both acute liver injury and chronic models of autoimmune hepatitis. celastrol 14-23 thymoma viral proto-oncogene 1 Mus musculus 106-110 35359864-10 2022 Conclusion: In summary, celastrol significantly attenuates autoimmune hepatitis by suppressing the PI3K/AKT signaling pathway, confirmed by validated animal models. celastrol 24-33 thymoma viral proto-oncogene 1 Mus musculus 104-107 35253615-0 2022 Celastrol, a TFEB (transcription factor EB) agonist, is a promising drug candidate for Alzheimer disease. celastrol 0-9 transcription factor EB Mus musculus 13-17 35253615-0 2022 Celastrol, a TFEB (transcription factor EB) agonist, is a promising drug candidate for Alzheimer disease. celastrol 0-9 transcription factor EB Mus musculus 19-42 35253615-7 2022 In a recent study, we showed that celastrol, a natural small molecule with an anti-obesity effect, is a novel TFEB activator, which enhances autophagy and lysosomal biogenesis both in vitro and in animal brains. celastrol 34-43 transcription factor EB Mus musculus 110-114 35253615-10 2022 Altogether, celastrol enhances TFEB-mediated autophagy and lysosomal biogenesis to ameliorate MAPT/tau pathology, suggesting that celastrol represents a novel anti-AD and other tauopathies drug candidate.Abbreviations: AD: Alzheimer disease; ALP: autophagy-lysosomal pathway; MAPT/tau: microtubule-associated protein tau; MTORC1: mechanistic target of rapamycin kinase complex 1; TFEB: transcription factor EB. celastrol 12-21 transcription factor EB Mus musculus 31-35 35253615-10 2022 Altogether, celastrol enhances TFEB-mediated autophagy and lysosomal biogenesis to ameliorate MAPT/tau pathology, suggesting that celastrol represents a novel anti-AD and other tauopathies drug candidate.Abbreviations: AD: Alzheimer disease; ALP: autophagy-lysosomal pathway; MAPT/tau: microtubule-associated protein tau; MTORC1: mechanistic target of rapamycin kinase complex 1; TFEB: transcription factor EB. celastrol 130-139 transcription factor EB Mus musculus 31-35 35051865-12 2022 In IMQ-induced psoriatic dermatitis, Cel gel reduced the secretion of interleukin (IL)- 23 by Langerhans cells, suppressed the interaction between Langerhans cells and gammadeltaT cells, and decreased the number of activated gammadeltaT cells and related IL-17 secretion, alleviating psoriasis-like inflammation. celastrol 37-40 interleukin 17A Mus musculus 255-260 35019905-5 2022 Celastrol was loaded into bovine serum albumin (BSA) nanoparticles to yield celastrol-BSA-NPs by high pressure homogenization. celastrol 0-9 albumin Mus musculus 33-46 35157199-0 2022 The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-kappab Signaling Pathways, and Inhibiting ERK Phosphorylation. celastrol 23-32 NFE2 like bZIP transcription factor 2 Rattus norvegicus 84-88 35157199-0 2022 The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-kappab Signaling Pathways, and Inhibiting ERK Phosphorylation. celastrol 23-32 heme oxygenase 1 Rattus norvegicus 89-93 35157199-0 2022 The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-kappab Signaling Pathways, and Inhibiting ERK Phosphorylation. celastrol 23-32 AKT serine/threonine kinase 1 Rattus norvegicus 100-103 35157199-0 2022 The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-kappab Signaling Pathways, and Inhibiting ERK Phosphorylation. celastrol 23-32 Eph receptor B1 Rattus norvegicus 180-183 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 NFE2 like bZIP transcription factor 2 Rattus norvegicus 58-101 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 NFE2 like bZIP transcription factor 2 Rattus norvegicus 103-107 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 heme oxygenase 1 Rattus norvegicus 109-125 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 heme oxygenase 1 Rattus norvegicus 127-131 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 AKT serine/threonine kinase 1 Rattus norvegicus 202-205 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 Eph receptor B1 Rattus norvegicus 267-304 35157199-2 2022 We investigated celastrol"s antioxidant potential through nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) and its effect on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, nuclear factor-kappa B (NF-kappaB) pathways, and extracellular signal-regulated kinase (ERK) activation in kidney ischemia-reperfusion injury (IRI) rat model. celastrol 16-25 Eph receptor B1 Rattus norvegicus 306-309 35157199-6 2022 Celastrol pretreatment attenuated oxidative stress and increased Nrf2 gene expression and HO-1 level. celastrol 0-9 NFE2 like bZIP transcription factor 2 Rattus norvegicus 65-69 35157199-6 2022 Celastrol pretreatment attenuated oxidative stress and increased Nrf2 gene expression and HO-1 level. celastrol 0-9 heme oxygenase 1 Rattus norvegicus 90-94 35157199-8 2022 Conclusively, celastrol showed a reno-protective potential against renal IRI by suppressing oxidative stress through enhancing the Nrf2/HO-1 pathway, augmenting cell survival PI3K/AKT signaling pathways, and reducing inflammation by inhibiting NF-kappaB activation. celastrol 14-23 NFE2 like bZIP transcription factor 2 Rattus norvegicus 131-135 35157199-8 2022 Conclusively, celastrol showed a reno-protective potential against renal IRI by suppressing oxidative stress through enhancing the Nrf2/HO-1 pathway, augmenting cell survival PI3K/AKT signaling pathways, and reducing inflammation by inhibiting NF-kappaB activation. celastrol 14-23 heme oxygenase 1 Rattus norvegicus 136-140 35157199-8 2022 Conclusively, celastrol showed a reno-protective potential against renal IRI by suppressing oxidative stress through enhancing the Nrf2/HO-1 pathway, augmenting cell survival PI3K/AKT signaling pathways, and reducing inflammation by inhibiting NF-kappaB activation. celastrol 14-23 AKT serine/threonine kinase 1 Rattus norvegicus 180-183 35138251-7 2022 On the other hand, celastrol-PEG4-alkyne was synthesized for identifying celastrol-bound proteins in RAW264.7 macrophages. celastrol 19-28 small nuclear ribonucleoprotein N Mus musculus 29-33 35138251-7 2022 On the other hand, celastrol-PEG4-alkyne was synthesized for identifying celastrol-bound proteins in RAW264.7 macrophages. celastrol 73-82 small nuclear ribonucleoprotein N Mus musculus 29-33 35138251-8 2022 ER chaperone GRP78 (78 kDa glucose-regulated protein) was identified by proteomics approach for celastrol binding to the residue Cys41. celastrol 96-105 heat shock protein 5 Mus musculus 13-18 35138251-8 2022 ER chaperone GRP78 (78 kDa glucose-regulated protein) was identified by proteomics approach for celastrol binding to the residue Cys41. celastrol 96-105 heat shock protein 5 Mus musculus 20-52 35138251-9 2022 Upon binding and conjugation, celastrol diminished the chaperone activity of GRP78 by 130-fold and reduced ER stress in palmitate-challenged cells, while celastrol analog lacking quinone methide failed to exhibit antiobesity effects. celastrol 30-39 heat shock protein 5 Mus musculus 77-82 35187141-8 2021 We also found that celastrol can upregulate Cleaved Caspase-3 and Cleaved Caspase-9 protein expression levels to promote cell apoptosis, and can regulate cell cycle-related proteins to induce cell cycle arrest. celastrol 19-28 caspase 3 Canis lupus familiaris 52-61 35187141-8 2021 We also found that celastrol can upregulate Cleaved Caspase-3 and Cleaved Caspase-9 protein expression levels to promote cell apoptosis, and can regulate cell cycle-related proteins to induce cell cycle arrest. celastrol 19-28 caspase 9 Canis lupus familiaris 74-83 35123623-0 2022 (Effect of Celastrol Based on IRAK4/ERK/p38 Signaling Pathway on Proliferation and Apoptosis of Multiple Myeloma Cells). celastrol 11-20 interleukin 1 receptor associated kinase 4 Homo sapiens 30-35 35134440-0 2022 Celastrol attenuates psoriasiform inflammation by targeting the IRF1/GSTM3 axis. celastrol 0-9 interferon regulatory factor 1 Homo sapiens 64-68 35134440-0 2022 Celastrol attenuates psoriasiform inflammation by targeting the IRF1/GSTM3 axis. celastrol 0-9 glutathione S-transferase mu 3 Homo sapiens 69-74 35113665-0 2022 Correction to: Celastrol Attenuates Angiotensin II-Induced Cardiac Remodeling by Targeting STAT3. celastrol 15-24 signal transducer and activator of transcription 3 Homo sapiens 91-96 35282664-10 2022 Significantly decreased macrophage infiltration, reduced levels of pro-inflammatory cytokines, increased level of anti-inflammatory cytokine and inhibited NF-kappaB signaling pathway were observed in the lung tissues of rats treated with celastrol. celastrol 238-247 nuclear factor kappa B subunit 1 Homo sapiens 155-164 35123623-9 2022 CONCLUSION: Celastrol can inhibit the proliferation and promote the apoptosis of H929 and ARP-1 cells, which may be related to inhibiting the phosphorylation of IRAK4 and blocking the activation of IRAK4/ERK/p38 signaling pathway. celastrol 12-21 actin related protein 1A Homo sapiens 90-95 35123623-0 2022 (Effect of Celastrol Based on IRAK4/ERK/p38 Signaling Pathway on Proliferation and Apoptosis of Multiple Myeloma Cells). celastrol 11-20 mitogen-activated protein kinase 1 Homo sapiens 36-39 35123623-9 2022 CONCLUSION: Celastrol can inhibit the proliferation and promote the apoptosis of H929 and ARP-1 cells, which may be related to inhibiting the phosphorylation of IRAK4 and blocking the activation of IRAK4/ERK/p38 signaling pathway. celastrol 12-21 interleukin 1 receptor associated kinase 4 Homo sapiens 161-166 35123623-0 2022 (Effect of Celastrol Based on IRAK4/ERK/p38 Signaling Pathway on Proliferation and Apoptosis of Multiple Myeloma Cells). celastrol 11-20 mitogen-activated protein kinase 14 Homo sapiens 40-43 35123623-9 2022 CONCLUSION: Celastrol can inhibit the proliferation and promote the apoptosis of H929 and ARP-1 cells, which may be related to inhibiting the phosphorylation of IRAK4 and blocking the activation of IRAK4/ERK/p38 signaling pathway. celastrol 12-21 interleukin 1 receptor associated kinase 4 Homo sapiens 198-203 35123623-9 2022 CONCLUSION: Celastrol can inhibit the proliferation and promote the apoptosis of H929 and ARP-1 cells, which may be related to inhibiting the phosphorylation of IRAK4 and blocking the activation of IRAK4/ERK/p38 signaling pathway. celastrol 12-21 mitogen-activated protein kinase 1 Homo sapiens 204-207 35123623-9 2022 CONCLUSION: Celastrol can inhibit the proliferation and promote the apoptosis of H929 and ARP-1 cells, which may be related to inhibiting the phosphorylation of IRAK4 and blocking the activation of IRAK4/ERK/p38 signaling pathway. celastrol 12-21 mitogen-activated protein kinase 14 Homo sapiens 208-211 35123623-10 2022 Celastrol combined with bortezomib has synergistic effect, which can more effectively inhibit the proliferation and induce apoptosis of H929 and ARP-1 cells. celastrol 0-9 actin related protein 1A Homo sapiens 145-150 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 40-49 mitogen-activated protein kinase 1 Homo sapiens 166-169 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 40-49 mitogen-activated protein kinase 14 Homo sapiens 170-173 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 196-205 interleukin 1 receptor associated kinase 4 Homo sapiens 160-165 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 196-205 mitogen-activated protein kinase 1 Homo sapiens 166-169 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 196-205 mitogen-activated protein kinase 14 Homo sapiens 170-173 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 294-303 interleukin 1 receptor associated kinase 4 Homo sapiens 160-165 35123623-1 2022 OBJECTIVE: To investigate the effect of celastrol on the proliferation and apoptosis of human multiple myeloma (MM) cell lines, reveal the relationship between IRAK4/ERK/p38 signaling pathway and celastrol regulating the proliferation and apoptosis of H929 and ARP-1 cells, and explore whether celastrol combined with bortezomib has synergistic effect. celastrol 294-303 mitogen-activated protein kinase 1 Homo sapiens 166-169 35123623-2 2022 METHODS: CCK-8 method was used to detect the viability of MM cell lines H929 and ARP-1 treated by different concentrations of celastrol, bortezomib, and their combination, and the synergistic effect was determined by Kim"s formula. celastrol 126-135 actin related protein 1A Homo sapiens 81-86 35141331-0 2022 Radiosensitizing Effect of Celastrol by Inhibiting G2/M Phase Arrest Induced by the c-myc Gene of Human SW1353 Chondrosarcoma Cells: Network and Experimental Analyses. celastrol 27-36 MYC proto-oncogene, bHLH transcription factor Homo sapiens 84-89 35123623-5 2022 RESULTS: Celastrol could significantly inhibit the proliferation of H929 and ARP-1 cells (r=0.9018, r=0.9244) and induce apoptosis in a time-dependent manner. celastrol 9-18 actin related protein 1A Homo sapiens 77-82 35141331-2 2022 This study is focused on the radiosensitization effect and apoptotic pathways of celastrol via the inhibition of the c-myc gene and the influence of which combined with radiotherapy on the proliferation, apoptosis, invasion, and metastasis of chondrosarcoma cells. celastrol 81-90 MYC proto-oncogene, bHLH transcription factor Homo sapiens 117-122 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 poly(ADP-ribose) polymerase 1 Homo sapiens 93-97 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 caspase 3 Homo sapiens 110-119 35141331-5 2022 Clone formation assay, CCK-8 assay, flow cytometry, and transwell migration assay were applied to detect the effects of celastrol on the expression of c-myc gene, cell apoptosis, and cell cycle. celastrol 120-129 MYC proto-oncogene, bHLH transcription factor Homo sapiens 151-156 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 interleukin 1 receptor associated kinase 4 Homo sapiens 160-165 35141331-8 2022 Celastrol can significantly inhibit the expression of the c-myc gene, induce G2/M phase arrest through regulation of G2/M phase-related proteins, and promote SW1353 cell apoptosis through the mitochondrial signaling pathway. celastrol 0-9 MYC proto-oncogene, bHLH transcription factor Homo sapiens 58-63 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 mitogen-activated protein kinase 1 Homo sapiens 169-172 35141331-10 2022 Conclusions: Our study validated the radiosensitization effect of celastrol through knocking down the expression of the c-myc gene to induce G2/M phase arrest and provides a new idea for the treatment of refractory or recurrent chondrosarcoma that is not sensitive to radiotherapy. celastrol 66-75 MYC proto-oncogene, bHLH transcription factor Homo sapiens 120-125 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 mitogen-activated protein kinase 14 Homo sapiens 180-183 35123623-6 2022 Compared with the control group, celastrol could significantly up-regulate the expression of PARP and cleaved caspase-3 while down-regulate the expression of p-IRAK4, p-ERK, and p-p38 in H929 and ARP-1 cells. celastrol 33-42 actin related protein 1A Homo sapiens 196-201 35123623-7 2022 Celastrol and bortezomib alone inhibited the proliferation of H929 and ARP-1 cells. celastrol 0-9 actin related protein 1A Homo sapiens 71-76 35273658-13 2022 Based on the potential of GDCA in PPPM, PARP-1 was found to be significantly correlated with the anticancer functions of celastrol. celastrol 121-130 poly(ADP-ribose) polymerase 1 Homo sapiens 40-46 35273658-15 2022 In addition, PARP-1 was found to be an important target of GDCA that promotes CRC; therefore, celastrol may be a potential targeted therapy for CRC via its effects on PARP-1. celastrol 94-103 poly(ADP-ribose) polymerase 1 Homo sapiens 13-19 35273658-15 2022 In addition, PARP-1 was found to be an important target of GDCA that promotes CRC; therefore, celastrol may be a potential targeted therapy for CRC via its effects on PARP-1. celastrol 94-103 poly(ADP-ribose) polymerase 1 Homo sapiens 167-173 35035665-0 2022 Celastrol Protects against Cerebral Ischemia/Reperfusion Injury in Mice by Inhibiting Glycolysis through Targeting HIF-1alpha/PDK1 Axis. celastrol 0-9 hypoxia inducible factor 1, alpha subunit Mus musculus 115-125 35022380-6 2022 HPA and GEPIA determined the expression of tripterine anti-ovarian hub genes in tumor tissues. celastrol 43-53 ELAV like RNA binding protein 2 Homo sapiens 67-70 35022380-11 2022 The expression of tripterine anti-ovarian hub genes ARHGAP11A, MUC1, and FUT8 were obtained by HPA and GEPIA. celastrol 18-28 ELAV like RNA binding protein 2 Homo sapiens 42-45 35022380-11 2022 The expression of tripterine anti-ovarian hub genes ARHGAP11A, MUC1, and FUT8 were obtained by HPA and GEPIA. celastrol 18-28 Rho GTPase activating protein 11A Homo sapiens 52-61 35022380-11 2022 The expression of tripterine anti-ovarian hub genes ARHGAP11A, MUC1, and FUT8 were obtained by HPA and GEPIA. celastrol 18-28 mucin 1, cell surface associated Homo sapiens 63-67 35022380-11 2022 The expression of tripterine anti-ovarian hub genes ARHGAP11A, MUC1, and FUT8 were obtained by HPA and GEPIA. celastrol 18-28 fucosyltransferase 8 Homo sapiens 73-77 35022380-14 2022 CONCLUSIONS Tripterine may be involved in megakaryocyte development and platelet production through potential genes ARHGAP11A, MUC1, HBB, RUNX1T1, and FUT8 and may have an anti-ovarian cancer effect in immune factors signaling, transporting and exchanging oxygen pathways, and autophagy pathways, through these 5 key genes. celastrol 12-22 Rho GTPase activating protein 11A Homo sapiens 116-125 35022380-14 2022 CONCLUSIONS Tripterine may be involved in megakaryocyte development and platelet production through potential genes ARHGAP11A, MUC1, HBB, RUNX1T1, and FUT8 and may have an anti-ovarian cancer effect in immune factors signaling, transporting and exchanging oxygen pathways, and autophagy pathways, through these 5 key genes. celastrol 12-22 mucin 1, cell surface associated Homo sapiens 127-131 35022380-14 2022 CONCLUSIONS Tripterine may be involved in megakaryocyte development and platelet production through potential genes ARHGAP11A, MUC1, HBB, RUNX1T1, and FUT8 and may have an anti-ovarian cancer effect in immune factors signaling, transporting and exchanging oxygen pathways, and autophagy pathways, through these 5 key genes. celastrol 12-22 hemoglobin subunit beta Homo sapiens 133-136 35022380-14 2022 CONCLUSIONS Tripterine may be involved in megakaryocyte development and platelet production through potential genes ARHGAP11A, MUC1, HBB, RUNX1T1, and FUT8 and may have an anti-ovarian cancer effect in immune factors signaling, transporting and exchanging oxygen pathways, and autophagy pathways, through these 5 key genes. celastrol 12-22 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 138-145 35022380-14 2022 CONCLUSIONS Tripterine may be involved in megakaryocyte development and platelet production through potential genes ARHGAP11A, MUC1, HBB, RUNX1T1, and FUT8 and may have an anti-ovarian cancer effect in immune factors signaling, transporting and exchanging oxygen pathways, and autophagy pathways, through these 5 key genes. celastrol 12-22 fucosyltransferase 8 Homo sapiens 151-155 35127390-5 2022 After loading celastrol into mannose-modified liposomes, they effectively inhibited the expression of maturation markers, including CD80, CD86 and MHC-II, on DCs both in vitro and in vivo. celastrol 14-23 CD80 antigen Mus musculus 132-136 35127390-5 2022 After loading celastrol into mannose-modified liposomes, they effectively inhibited the expression of maturation markers, including CD80, CD86 and MHC-II, on DCs both in vitro and in vivo. celastrol 14-23 CD86 antigen Mus musculus 138-142 35127390-5 2022 After loading celastrol into mannose-modified liposomes, they effectively inhibited the expression of maturation markers, including CD80, CD86 and MHC-II, on DCs both in vitro and in vivo. celastrol 14-23 histocompatibility-2, MHC Mus musculus 147-153 35035665-0 2022 Celastrol Protects against Cerebral Ischemia/Reperfusion Injury in Mice by Inhibiting Glycolysis through Targeting HIF-1alpha/PDK1 Axis. celastrol 0-9 pyruvate dehydrogenase kinase, isoenzyme 1 Mus musculus 126-130 35035665-10 2022 In addition, celastrol significantly blocked I/R-induced increase of LDHA, GLUT1, HK2, and lactate production as well as decrease of ATP level and glucose content. celastrol 13-22 lactate dehydrogenase A Mus musculus 69-73 35035665-10 2022 In addition, celastrol significantly blocked I/R-induced increase of LDHA, GLUT1, HK2, and lactate production as well as decrease of ATP level and glucose content. celastrol 13-22 solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus 75-80 35035665-10 2022 In addition, celastrol significantly blocked I/R-induced increase of LDHA, GLUT1, HK2, and lactate production as well as decrease of ATP level and glucose content. celastrol 13-22 hexokinase 2 Mus musculus 82-85 35035665-11 2022 Moreover, celastrol inhibited the I/R-induced upregulation of HIF-1alpha and PDK1. celastrol 10-19 hypoxia inducible factor 1, alpha subunit Mus musculus 62-72 35035665-11 2022 Moreover, celastrol inhibited the I/R-induced upregulation of HIF-1alpha and PDK1. celastrol 10-19 pyruvate dehydrogenase kinase, isoenzyme 1 Mus musculus 77-81 35035665-12 2022 Overexpression of HIF-1alpha by DMOG reversed the protective effect of celastrol on cerebral I/R injury and blocked celastrol-induced suppression of glycolysis. celastrol 71-80 hypoxia inducible factor 1, alpha subunit Mus musculus 18-28 35035665-12 2022 Overexpression of HIF-1alpha by DMOG reversed the protective effect of celastrol on cerebral I/R injury and blocked celastrol-induced suppression of glycolysis. celastrol 116-125 hypoxia inducible factor 1, alpha subunit Mus musculus 18-28 35035665-14 2022 Taken together, these results suggested that celastrol protected against cerebral I/R injury through inhibiting glycolysis via the HIF-1alpha/PDK1 axis. celastrol 45-54 hypoxia inducible factor 1, alpha subunit Mus musculus 131-141 35035665-14 2022 Taken together, these results suggested that celastrol protected against cerebral I/R injury through inhibiting glycolysis via the HIF-1alpha/PDK1 axis. celastrol 45-54 pyruvate dehydrogenase kinase, isoenzyme 1 Mus musculus 142-146 34918393-7 2022 Subsequently, we confirmed that two medicinal plant-derived compounds, andrographolide, and celastrol, widely used as a nutritional or medicinal supplement are useful to attenuate DENV-induced plasma leakage through induction of the HO-1 expression in DENV-infected AG129 mice. celastrol 92-101 heme oxygenase 1 Homo sapiens 233-237 35466134-4 2022 Increase in MAFbx1/atrogin-1 and MuRF-1 by 3D-clinorotation was significantly suppressed by treatment with C14-Cblin or celastrol, but there was no additive effect of simultaneous treatment. celastrol 120-129 F-box protein 32 Rattus norvegicus 19-28 35466134-4 2022 Increase in MAFbx1/atrogin-1 and MuRF-1 by 3D-clinorotation was significantly suppressed by treatment with C14-Cblin or celastrol, but there was no additive effect of simultaneous treatment. celastrol 120-129 tripartite motif containing 63 Rattus norvegicus 33-39 35466134-5 2022 However, celastrol significantly suppressed the upregulation of Cbl-b and HSP70 by 3D-clinorotation. celastrol 9-18 Cbl proto-oncogene B Rattus norvegicus 64-69 35466134-5 2022 However, celastrol significantly suppressed the upregulation of Cbl-b and HSP70 by 3D-clinorotation. celastrol 9-18 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 74-79 35466134-6 2022 Whereas 3D-clinorotation decreased the protein level of IRS-1 in L6 myotubes, C14-Cblin and celastrol inhibited the degradation of IRS-1. celastrol 92-101 insulin receptor substrate 1 Rattus norvegicus 131-136 35466134-7 2022 C14-Cblin and celastrol promoted the phosphorylation of FOXO3a even in microgravity condition. celastrol 14-23 forkhead box O3 Rattus norvegicus 56-62