PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 29631379-11 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 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 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 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 29493374-11 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 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 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 25310109-3 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 25310109-5 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 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 25116125-5 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 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 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 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 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 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 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 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 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 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