PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 33740524-8 2021 Furthermore, AETC reduced the tumor volume and weight in nude mice; upregulated ATF3, p-MOB1, and p-YAP (Ser397); and actively regulated cleaved PARP and cleaved caspase-9/8/3. aetc 13-17 caspase 9 Mus musculus 162-175 34058674-9 2021 Additionally, Rb1 significantly reversed the DON-induced excessive splenic apoptosis via modulating the mitochondria-mediated apoptosis pathway in mice, depicting the decreased percentage of splenocyte apoptotic cells by 26.65%, down-regulated the mRNA abundance of Bax, caspase-3, caspase-9, and protein expression of Bax, cleaved caspase-3, and Cyt-c. deoxynivalenol 45-48 caspase 9 Mus musculus 282-291 33646450-5 2021 Cisplatin-induced cell damages were evaluated by TUNEL assay and immunoblot analyses for p53, 14-3-3, Bax, Bcl2, cytochrome C, and activated caspases. Cisplatin 0-9 caspase 9 Mus musculus 141-149 33646450-7 2021 RESULTS: GW0742 suppressed cisplatin-induced apoptosis of mProx cells by reducing the activation of caspase-3 via attenuating the phosphorylation of p53 and 14-3-3, mitochondrial Bax accumulation, cytochrome C release from mitochondria to the cytosol and ensuing cytosolic caspase-9 activation. GW0742 9-15 caspase 9 Mus musculus 273-282 33646450-7 2021 RESULTS: GW0742 suppressed cisplatin-induced apoptosis of mProx cells by reducing the activation of caspase-3 via attenuating the phosphorylation of p53 and 14-3-3, mitochondrial Bax accumulation, cytochrome C release from mitochondria to the cytosol and ensuing cytosolic caspase-9 activation. Cisplatin 27-36 caspase 9 Mus musculus 273-282 33921050-11 2021 In addition, we also observed a significant fold reduction (p < 0.05) in ROS fluorescent intensity and the expression of Bax (p < 0.0001), cytochrome C (p < 0.0001), cleaved caspase-9 (p > 0.010) and cleaved caspase-3 (p < 0.0001). Reactive Oxygen Species 73-76 caspase 9 Mus musculus 174-183 34002388-8 2021 BPS also significantly upregulated cleaved caspase-8, cleaved caspase-9, cleaved caspase-3, Fas, and FasL and significantly downregulated the Bcl-2/Bax ratio. bis(4-hydroxyphenyl)sulfone 0-3 caspase 9 Mus musculus 62-71 33652185-8 2021 In vitro, the mimic of miRNA-450 b-3p reversed the decrease of viability and the increase of apoptosis rate and significantly antagonized the expression enhancements of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, Caspase-3 induced by SiNPs, while inhibitor of miRNA-450 b-3p further promoted the effects induced by SiNPs. mirna-450 b-3p 23-37 caspase 9 Mus musculus 204-213 33713642-2 2021 One of the most principal mechanisms of its ototoxicity is that GM can activate caspase-mediated cell death pathways in the cochlea. Gentamicins 64-66 caspase 9 Mus musculus 80-87 33438769-5 2021 Results indicated that BPA-treated animals demonstrated a marked decrease in antioxidant enzyme activities (superoxide dismutase, catalase, redox ratio), a marked elevation in the expressions of stress-activated kinases (c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38) and the expressions of pro-apoptotic markers (caspase-9, caspase-8 and caspase-3). bisphenol A 23-26 caspase 9 Mus musculus 353-362 33713642-3 2021 Since the anti-apoptotic protein known as X-linked Inhibitor of Apoptosis Protein (XIAP) has been reported to directly bind to activated caspase protein and inhibit their activities, we hypothesized that it might protect cochlea hair cells from GM ototoxicity. Gentamicins 245-247 caspase 9 Mus musculus 137-144 33217075-5 2021 In addition, xanthomicrol reduced the expression of TNFalpha, VEGF, MMP9, and Ki67, while upregulating the expression of apoptotic markers such as Bax, caspase3, and caspase9. xanthomicrol 13-25 caspase 9 Mus musculus 166-174 33713642-7 2021 Finally, immunofluorescence assays were used to detect the effect of GM on the expression of caspase protein and verify the protective effect of XIAP. Gentamicins 69-71 caspase 9 Mus musculus 93-100 33713642-8 2021 We found that GM at a concentration of 0.5 mM significantly affected the function of cochlea hair cells, up-regulating the expression of cleaved-caspase-3 and cleaved-caspase-9 protein but down-regulating XIAP protein. Gentamicins 14-16 caspase 9 Mus musculus 167-176 33545631-8 2021 In vitro studies further confirmed that high glucose (HG) induced mitochondrial dysfunction, along with enhanced releases of Cyto-c from mitochondria and elevated expression of cleaved Caspase-9, contributing to intrinsic apoptosis in podocytes. Glucose 45-52 caspase 9 Mus musculus 185-194 33678756-3 2021 The results indicated that treatment with SRT1720 inhibited LPS/D-Gal-induced elevation of ALT and AST, alleviated the histological abnormalities, suppressed the induction of TNF-alpha and IL-6, mitigated the phosphorylation of JNK, downregulated the activities of caspase 8, caspase 9 and caspase 3, decreased the level of cleaved caspase 3, reduced the TUNEL-positive cells, and improved the survival rate of the LPS/D-Gal-exposed mice. SRT1720 42-49 caspase 9 Mus musculus 276-285 33586527-0 2022 Radix Tetrastigma Inhibits the Non-Small Cell Lung Cancer via Bax/Bcl-2/Caspase-9/Caspase-3 Pathway. tetrastigma 6-17 caspase 9 Mus musculus 72-81 33678756-3 2021 The results indicated that treatment with SRT1720 inhibited LPS/D-Gal-induced elevation of ALT and AST, alleviated the histological abnormalities, suppressed the induction of TNF-alpha and IL-6, mitigated the phosphorylation of JNK, downregulated the activities of caspase 8, caspase 9 and caspase 3, decreased the level of cleaved caspase 3, reduced the TUNEL-positive cells, and improved the survival rate of the LPS/D-Gal-exposed mice. Galactose 64-69 caspase 9 Mus musculus 276-285 33609891-8 2021 Meanwhile, GLN significantly increased the activities of Caspase-3, Caspase-8, caspase-9 and PARP. Glutamine 11-14 caspase 9 Mus musculus 79-88 33044639-9 2021 However, selenium treatment diminished activations of TRPM2, cytokine, Casp-3, and Casp-9, and levels of lipid peroxidation and mitochondrial ROS production in the microglia that were treated with IFNgamma. Selenium 9-17 caspase 9 Mus musculus 83-89 33044639-19 2021 The main mechanism in the cell death and inflammatory effects of IFNgamma is mediated by stimulation of ROS-mediated caspase (caspase -3 and - 9) activations and cytokine production (TNF-alpha, IL-1beta, and IL-6) via TRPM2 activation, respectively. Reactive Oxygen Species 104-107 caspase 9 Mus musculus 117-124 32920884-8 2020 In contrast, the expression of apoptotic markers including caspase 3, caspase 9 and Bax was increased in the presence of MK801. Dizocilpine Maleate 121-126 caspase 9 Mus musculus 70-79 33575163-13 2021 Compared with the LPS group, APS pretreatment could inhibit the expression of inflammatory factors including TNF-alpha, IL-1 beta, IL-6, and IL-8 (all P < 0.05), reducing the number of apoptotic cells (P < 0.05), suppressing the expression of caspase-3, caspase-9, and Bax, but upregulating the expression levels of Bcl-2. aps 29-32 caspase 9 Mus musculus 254-263 33494783-12 2021 Western blot showed that application of Pt-MWNTS can significantly upregulate the expression level of Bax, Bim, Bid, Caspase-3 and Caspase-9 while downregulate the expression level of Bcl-2, compared with free cisplatin. Platinum 40-42 caspase 9 Mus musculus 131-140 33396178-6 2021 Cd significantly down-regulated caspase 9 and induced cleaved-PARP, cleaved-caspase 3 protein level. Chlorides 0-2 caspase 9 Mus musculus 32-41 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 9 Mus musculus 14-21 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 9 Mus musculus 31-38 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 50-59 caspase 9 Mus musculus 145-154 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. Cadmium 103-110 caspase 9 Mus musculus 14-21 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. Cadmium 103-110 caspase 9 Mus musculus 31-38 33396178-8 2021 Inhibition of caspase with pan-caspase inhibitor, Z-VAD-FMK, prevented MC3T3-E1 subclone 14 cells from cadmium-induced reduction of Runx2, STC2, caspase 9, and accumulation of cleaved PARP and cleaved caspase 3. Cadmium 103-110 caspase 9 Mus musculus 145-154 33396178-10 2021 These results suggest that cadmium cytotoxicity on bone involved exportin 1 accumulation, phosphorylation of JNK, induction of DNA damage and pro-apoptosis, which was induced by activation of caspase-dependent pathways. Cadmium 27-34 caspase 9 Mus musculus 192-199 33519423-8 2020 Western blotting revealed a decrease in cleaved caspase-9 and caspase-3 expression in line with ROS levels. ros 96-99 caspase 9 Mus musculus 48-57 33490128-7 2020 Quercetin supplementation also inhibited the activities of caspases-9 and-3, and the expression of p53 and Bax mRNAs. Quercetin 0-9 caspase 9 Mus musculus 59-75 33365077-11 2021 In addition, the expression of survivin and XIAP was significantly downregulated, whereas the expression of caspase-3, caspase-7 and caspase-9 was significantly upregulated in tumor tissues from nude mice treated with matrine + cisplatin, compared with those treated with cisplatin, matrine or normal saline. matrine 218-225 caspase 9 Mus musculus 133-142 33365077-11 2021 In addition, the expression of survivin and XIAP was significantly downregulated, whereas the expression of caspase-3, caspase-7 and caspase-9 was significantly upregulated in tumor tissues from nude mice treated with matrine + cisplatin, compared with those treated with cisplatin, matrine or normal saline. Cisplatin 228-237 caspase 9 Mus musculus 133-142 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. matrine 49-56 caspase 9 Mus musculus 138-145 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. matrine 49-56 caspase 9 Mus musculus 218-227 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. Cisplatin 61-70 caspase 9 Mus musculus 138-145 33365077-12 2021 These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9. Cisplatin 61-70 caspase 9 Mus musculus 218-227 33332077-6 2020 Dex treatment also increased cell viability, reduced apoptotic ratio and downregulated expression levels of Cleaved Caspase-3 and Cleaved Caspase-9 in H/R induced MPVECs. Dexmedetomidine 0-3 caspase 9 Mus musculus 138-147 33187346-11 2020 It also inhibited the apoptotic cell death through the inhibition of cytochrome c release and cleaved caspase-9, -3 in glutamate-treated HT22 cells. Glutamic Acid 119-128 caspase 9 Mus musculus 102-111 33045563-8 2020 Moreover, in the renal tissues of LIGHT KO mice, cisplatin-induced mitochondrion injury and the levels of the pro-apoptotic molecules Bax, Cytochrome C (Cyt C), cleaved caspase-3, and cleaved caspase-9 were dramatically increased; in contrast, the expression of anti-apoptotic molecule Bcl-2 was markedly reduced, compared to those in WT mice, suggesting that LIGHT deficiency accelerated cisplatin-induced mitochondrial apoptosis of renal tubular cells in these mice. Cisplatin 49-58 caspase 9 Mus musculus 192-201 32515636-9 2020 In addition, BisPH-A induced mitochondrial membrane depolarization, reactive oxygen species (ROS), caspase 3, caspase 9 and apoptosis values were decreased by the resveratrol treatment. bisphenol A 13-20 caspase 9 Mus musculus 110-119 32515636-9 2020 In addition, BisPH-A induced mitochondrial membrane depolarization, reactive oxygen species (ROS), caspase 3, caspase 9 and apoptosis values were decreased by the resveratrol treatment. Resveratrol 163-174 caspase 9 Mus musculus 110-119 33211772-8 2020 Consequently, fragmented mitochondria lost their membrane integrity and ROS was accumulated to trigger caspase 9-dependent apoptosis before autophagic rescue. ros 72-75 caspase 9 Mus musculus 103-112 32918989-8 2020 Furthermore, ASX markedly upregulated the expression of Bcl-2 and downregulated the expressions of Fas, FasL, RIPK1, FADD, Bax, Cytochrome C, Caspase-9, Cleaved Caspase-8, Cleaved Caspase-3, RIPK3, MLKL and FLIP in the testis tissues compared with the NF group. astaxanthine 13-16 caspase 9 Mus musculus 142-151 32809047-8 2020 SD also promoted LPS/D-Gal-induced production of TNF-alpha and upregulated hepatic caspase-8, caspase-9, and caspase-3 activities in LPS/D-Gal-exposed mice. Galactose 21-26 caspase 9 Mus musculus 94-103 32589884-7 2020 Further elucidation of the mechanism revealed that 6H2L induced mitochondrial dysfunction, with transmitochondrial membrane potential collapse and cytochrome c release, which activated caspase-9 and caspase-3 and subsequently cleaved PARP, suggesting that 6H2L induced apoptosis via triggering mitochondrial pathway. 6h2l 51-55 caspase 9 Mus musculus 185-194 33312522-8 2020 p-AKT, caspase-3, and caspase-9 protein expression was stimulated in the model group but was depressed in the AST-treated groups. ast 110-113 caspase 9 Mus musculus 22-31 32569717-7 2020 AIM OF THE STUDY: To investigate the protective effect of PS against cadmium-induced testicular injury in mice via the TXNIP-NLRP3-Caspase-1 and CytC-Caspase-9-Caspase-3 pathway. ps 58-60 caspase 9 Mus musculus 150-159 33100110-8 2022 Moreover, MOR treatment caused a significant increase in bcl-2 expression, and obvious decreases in the expression levels of bax, cleaved caspase-3, and cleaved caspase-9 expression. morroniside 10-13 caspase 9 Mus musculus 161-170 33059637-4 2020 The inhibitory pathway of anthocyanin was explored by assessment of tumour cell mitochondrial membrane potential (MMP), the caspase-3 and caspase-9 activity, as well as the cell energy metabolism in terms of the glucose uptake, the NAD+/NADH ratio and the ATP level. Anthocyanins 26-37 caspase 9 Mus musculus 138-147 33059637-5 2020 RESULTS: We found that 500 muM bilberry anthocyanins extract (BAE) induced 48.1% mitochondrial damage, activated the downstream caspase cascade to form apoptotic bodies (caspase-3 activity increased by 169%, caspase-9 activity increased by 186%), and inhibited cell proliferation (survival rate: 55.97%, 24 h). anthocyanins extract 40-60 caspase 9 Mus musculus 208-217 33178764-11 2020 beta-elemene promoted cell apoptosis, with increased expression of cleaved caspase-9 and decreased BCL-2 expression. beta-elemene 0-12 caspase 9 Mus musculus 75-84 32717422-9 2020 Suppression of cell viability, increase of cytotoxicity, induction of apoptosis, alteration in the expression of apoptotic-related proteins, and activation of caspase-3 and caspase-9 were shown in matrine-treated NCTC cells. matrine 197-204 caspase 9 Mus musculus 173-182 32589884-7 2020 Further elucidation of the mechanism revealed that 6H2L induced mitochondrial dysfunction, with transmitochondrial membrane potential collapse and cytochrome c release, which activated caspase-9 and caspase-3 and subsequently cleaved PARP, suggesting that 6H2L induced apoptosis via triggering mitochondrial pathway. 6h2l 256-260 caspase 9 Mus musculus 185-194 32656716-12 2020 Moreover, licoricidin decreased the TUNEL positive neurons, downregulated the expression of Cyt-C, cleaved-Caspase-3, cleaved-Caspase-9 and Bax and upregulated the Bcl-2, attenuated cellular apoptosis. licoricidin 10-21 caspase 9 Mus musculus 126-135 32768939-7 2020 LBZ activates PI3K/Akt signaling pathways and granulocyte-colony-stimulating-factor (G-CSF)-mediated Janus kinase 2 (JAK2)/transcription 3 (STAT3), resulting in inhibiting the release of cytochrome c. Further, LBZ inhibits caspase-mediated mitochondrial-dependent apoptosis mediated by caspase-9 and caspase-3. lbz 0-3 caspase 9 Mus musculus 223-230 32768939-7 2020 LBZ activates PI3K/Akt signaling pathways and granulocyte-colony-stimulating-factor (G-CSF)-mediated Janus kinase 2 (JAK2)/transcription 3 (STAT3), resulting in inhibiting the release of cytochrome c. Further, LBZ inhibits caspase-mediated mitochondrial-dependent apoptosis mediated by caspase-9 and caspase-3. lbz 0-3 caspase 9 Mus musculus 286-295 32963966-6 2020 As expected, CdCl2 remarkably induced loss of histological integrity, increased DNA comet formation, increased TNF-alpha and p53 mRNA expression levels and increased the immunoreactivity of caspase-9 expression. Cadmium Chloride 13-18 caspase 9 Mus musculus 190-199 32759462-6 2020 Meanwhile, the expressions of pro-apoptotic markers, which were BAX and CASPASEs (CASPASE-9 and CASPASE-3), were prominently reduced in Esculentoside A-induced premature ovarian failure mice. esculentoside A 136-151 caspase 9 Mus musculus 82-91 32535761-6 2020 MPP-induced increases in apoptosis, death, OS, lipid peroxidation, PARP1, caspase-3 and caspase-9, inflammatory cytokines (IL-1beta, TNF-alpha, IL-6), and intracellular free Zn2+ and Ca2+ levels in the microglia of TRPM2-WT mice were further increased by the BSO treatment, although they were diminished by the GSH treatment. mangion-purified polysaccharide (Candida albicans) 0-3 caspase 9 Mus musculus 88-97 32848758-5 2020 Both in vivo and in vitro results demonstrated that 7-HC alleviated oxidative stress and apoptosis induced by colistin, as shown by decreased malondialdehyde levels, decreased caspase-3 and caspase-9 activities, and increased superoxide dismutase and catalase activities. 7-hydroxycoumarin 52-56 caspase 9 Mus musculus 190-199 32650488-5 2020 CuSO4 exposure up-regulated the activities and mRNA expression of caspases-9 and -3 as well as the expression of glucose-regulated protein 78 (GRP78), GRP94, DNA damage-inducible gene 153 (GADD153/CHOP), caspase-12 mRNAs in the kidney tissues. Copper Sulfate 0-5 caspase 9 Mus musculus 66-83 32471877-6 2020 We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections. Cesium 144-146 caspase 9 Mus musculus 78-87 32471877-6 2020 We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections. Cesium 144-146 caspase 9 Mus musculus 207-216 32471877-6 2020 We further show that mice that lack the activity-dependent Bax/Bak pathway or caspase-9 similarly exhibit defects in elimination of ipsilateral CS projections, suggesting that the activity-dependent Bax/Bak-caspase-9 pathway is essential for the removal of ipsilateral CS projections. Cesium 269-271 caspase 9 Mus musculus 207-216 32952128-5 2020 Also, CuSO4 induced apoptosis, which was accompanied by decreasing Bcl-2, Bcl-xL mRNA expression levels and protein expression levels, and increasing Bax, Bak, cleaved-caspase-3, cleaved-caspase-9 mRNA, and protein expression levels, and Bax/Bcl-2 ratio. Copper Sulfate 6-11 caspase 9 Mus musculus 187-196 32344356-4 2020 RESULTS: Our findings confirmed that cafestol preconditioning groups could reduce the levels of ALT and AST, alleviate liver pathological damage, suppress the release of inflammation mediators, inhibit the production of pro-apoptosis protein including caspase-3, caspase-9 and Bax, decrease the expression of autophagy-linked protein including Beclin-1 and LC3, increase anti-apoptosis protein Bcl-2, and restrain the activation of ERK and PPARgamma. cafestol 37-45 caspase 9 Mus musculus 263-272 32361189-9 2020 Importantly, hydrogen treatment prevented mitochondrial depolarization, cytochrome c release, and activity of caspase-3, caspase-9, and PARP. Hydrogen 13-21 caspase 9 Mus musculus 121-130 32907306-6 2020 The results found that NMDA can increase the oxidative stress of HT22 cells in a dose-dependent manner, downregulate the expression of miR-382-3p, upregulate the expression of mRNA and protein abundance of ROCK1 and RhoC, increase the expression levels of proapoptotic proteins Bax, Caspase-3, and Caspase-9, increase the apoptosis of HT22 cells, and reduce the activity and survival rate of HT22 cells. N-Methylaspartate 23-27 caspase 9 Mus musculus 298-307 32907306-7 2020 Compared with the NMDA-induced group, the miR-382-3p mimic-transfected HT22 cells increased the expression of miR- 382-3p, reduced the expression of the mRNA and protein abundance of ROCK1 and RhoC, inhibited the expression of proapoptotic proteins Bax, Caspase-3, and Caspase-9, reduced the apoptosis of HT22 cells, and increased the activity and survival rate of HT22 cells. N-Methylaspartate 18-22 caspase 9 Mus musculus 269-278 32566100-11 2020 Taurine significantly increased the levels of an apoptosis marker cleaved caspase-9 and tumor suppressor protein PTEN. Taurine 0-7 caspase 9 Mus musculus 74-83 32278173-11 2020 The mRNA expression levels of Cyt c, caspase 9 and 3 markedly increased in the fluoride treated groups in a dose-dependent manner. Fluorides 79-87 caspase 9 Mus musculus 37-52 32571324-8 2020 The data showed that ASP decreased damage to the mitochondrial outer membrane, improved the stabilization of the mitochondrial membrane, and corrected the abnormal levels of ROS and mitochondrial-associated apoptosis proteins, including the Bcl-2/Bax ratio and caspase-3 and caspase-9 expression, in BMNCs which were sorted from the bone marrow cells of AA mice. Aspartic Acid 21-24 caspase 9 Mus musculus 275-284 31927655-11 2020 In addition, DEX dramatically prevented sepsis-induced pulmonary cell apoptosis in mice, as reflected by decreases in the number of TUNEL-positive cells, the protein expression of cleaved caspase-9 and cleaved caspase 3 and the Bax/Bcl-2 ratio. Dexmedetomidine 13-16 caspase 9 Mus musculus 188-197 32265302-3 2020 Here, we report that atRAL activates c-Jun N-terminal kinase (JNK) signaling at least partially through reactive oxygen species (ROS) production, which promoted mitochondria-mediated caspase- and DNA damage-dependent apoptosis in photoreceptor cells. Reactive Oxygen Species 104-127 caspase 9 Mus musculus 183-190 32265302-3 2020 Here, we report that atRAL activates c-Jun N-terminal kinase (JNK) signaling at least partially through reactive oxygen species (ROS) production, which promoted mitochondria-mediated caspase- and DNA damage-dependent apoptosis in photoreceptor cells. Reactive Oxygen Species 129-132 caspase 9 Mus musculus 183-190 32543135-14 2020 Compared with the control group, in the three groups that treated with DDP, the formation of clones and the expression of proliferation marker proteins Ki67 and PCNA were reduce ( P<0.01), while the rate of apoptosis and the expression of apoptosis marker proteins Caspase-3 and Caspase-9 were increased ( P<0.01). Cisplatin 71-74 caspase 9 Mus musculus 279-288 32256652-13 2020 The antiapoptosis effect of EPS was through reversing apoptotic proteins such as BAX, Caspase-9 and Caspase-3, and Bcl-2. eps 28-31 caspase 9 Mus musculus 86-95 32037797-7 2020 Curcumin supplementation at 200 mg/kg up-regulated the levels of AKT, NGF, mTOR, Nrf2 and HO-1 mRNA, and concomitantly down-regulated Bax, caspases-3 and -9 mRNA; it also decreased caspase-3 and caspase-9 activity. Curcumin 0-8 caspase 9 Mus musculus 195-204 31912924-6 2020 mRNA expression study revealed significant decrease in the expression of Bcl-2 and increase in expressions of caspase-9 and caspase-3, thus clearly demonstrate BPA-induced apoptosis. bisphenol A 160-163 caspase 9 Mus musculus 110-119 32190177-10 2020 ASX played a protective role by changing the expression of Keap1, Nrf2, HO-1, Bax, Bcl-2, Caspase3, and Caspase9 proteins. astaxanthine 0-3 caspase 9 Mus musculus 104-112 31830590-6 2020 The proapoptotic effect of GA involved the increased phosphorylation of p38 and JNK1/2; increased cleavage of caspase 3, caspase 9 and PARP; reduced phosphorylation of mTOR, Akt and ERK1/2; and reduced expressions of survivin and cyclin D1. Glycyrrhetinic Acid 27-29 caspase 9 Mus musculus 121-130 31808042-4 2020 Linagliptin up-regulated the expression of p-Akt and p-mTOR and regulated the apoptosis factors Bcl-2, Bax, and caspase 9. linagliptin 0-11 caspase 9 Mus musculus 112-121 31918714-6 2020 Subsequently, TPH/PTX caused mitochondrial outer membrane permeabilization (MOMP) by inhibiting antiapoptotic Bcl-2, leading to cytochrome C release and activation of caspase-3 and caspase-9. Paclitaxel 18-21 caspase 9 Mus musculus 181-190 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 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. Metformin 46-55 caspase 9 Mus musculus 138-147 32172946-7 2020 Furthermore, DP pretreatment could inhibit the apoptosis of liver cells caused by APAP through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 protein. dp 13-15 caspase 9 Mus musculus 149-158 31834612-10 2020 Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases. Tunicamycin 28-30 caspase 9 Mus musculus 55-64 31834612-10 2020 Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases. Tunicamycin 28-30 caspase 9 Mus musculus 171-179 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 130-132 caspase 9 Mus musculus 169-177 31874178-6 2020 Expressions of apoptosis-related proteins including bax, cyt-c, and caspase-9 were significantly up-regulated by exposure to 2.5, 5, 10, or 20 mug MC-LR/mL. cyanoginosin LR 147-152 caspase 9 Mus musculus 68-77 31593881-7 2020 BPA also increased the relative expression of caspase-7, caspase-9, bax, inhibited the relative expression of bcl-2 in F1 females at both PND 21 and 56, and increased the apoptosis rate in the ovaries in F1 mice at PND 56 (P < 0.01). bisphenol A 0-3 caspase 9 Mus musculus 57-66 32990004-6 2020 RESULTS: Memantine altered the Bcl-2, Bax, Casp3, Casp-9 apoptotic protein expression levels. Memantine 9-18 caspase 9 Mus musculus 50-56 31841689-7 2020 Reactive oxygen species (ROS) inside RAW264.7 cells after SDT led to the decrease of mitochondrial membrane potential (MMP) and the higher expression of cleaved caspase-9/3. Reactive Oxygen Species 0-23 caspase 9 Mus musculus 161-172 31841689-7 2020 Reactive oxygen species (ROS) inside RAW264.7 cells after SDT led to the decrease of mitochondrial membrane potential (MMP) and the higher expression of cleaved caspase-9/3. Reactive Oxygen Species 25-28 caspase 9 Mus musculus 161-172 33480238-9 2020 Furthermore, amifostine suppressed neuronal apoptosis, accompanied by the reduction of Bax, cleaved caspase-9, cleaved caspase-3, and Bcl-2 upregulation. Amifostine 13-23 caspase 9 Mus musculus 100-109 31660692-6 2020 To further explore the mechanism of autophagy on macrophage apoptosis, we used macrophage apoptosis model in vitro and found that 7-ketocholesterol (7-KC, one of the primary oxysterols in oxLDL) caused macrophage apoptosis with concomitant impairment of mitochondria, characterized by the impairment of mitochondrial ultrastructure, cytochrome c release, mitochondrial potential dissipation, mitochondrial fragmentation, excessive ROS generation and both caspase-9 and caspase-3 activation. 7-ketocholesterol 130-147 caspase 9 Mus musculus 455-464 32749127-4 2020 We determined experimentally that naringin pretreatment prevents UVB-induced nuclear fragmentation in NIH-3T3 cells, as well as altering UVB-induced apoptotic marker (Bax, BCl-2, Caspase-9, and Caspase-3) expression in them. naringin 34-42 caspase 9 Mus musculus 179-188 31660692-6 2020 To further explore the mechanism of autophagy on macrophage apoptosis, we used macrophage apoptosis model in vitro and found that 7-ketocholesterol (7-KC, one of the primary oxysterols in oxLDL) caused macrophage apoptosis with concomitant impairment of mitochondria, characterized by the impairment of mitochondrial ultrastructure, cytochrome c release, mitochondrial potential dissipation, mitochondrial fragmentation, excessive ROS generation and both caspase-9 and caspase-3 activation. 7-ketocholesterol 149-153 caspase 9 Mus musculus 455-464 31563530-7 2019 PCB126 could increase protein expression of Bax, Caspase-3, Caspase-8 and Caspase-9, while the protein expression of Bcl-2 was decreased. 3,4,5,3',4'-pentachlorobiphenyl 0-6 caspase 9 Mus musculus 74-83 31638199-8 2019 LY294002 further enhanced Ang II-induced downregulation of Akt and p65 NF-kappaB activation, as well as upregulation of caspase-9 mRNA and protein, and promoted the apoptosis of podocytes. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 0-8 caspase 9 Mus musculus 120-129 31638199-9 2019 Of note, 740Y-P restored Ang II-induced downregulation of Akt and p65 NF-kappaB activation, and upregulation of caspase-9, and decreased podocyte apoptosis. 740y-p 9-15 caspase 9 Mus musculus 112-121 31673102-10 2019 TG and Api combination induced caspase-8 and caspase-9 dependent apoptosis. Thapsigargin 0-2 caspase 9 Mus musculus 45-54 31673102-10 2019 TG and Api combination induced caspase-8 and caspase-9 dependent apoptosis. apicidin 7-10 caspase 9 Mus musculus 45-54 31131920-6 2019 Increased lipid peroxidation, ROS, apoptosis, caspase-3 and caspase-9 activities in the kidney and testes of the DTX group were diminished by treatment with MEL and Se. Docetaxel 113-116 caspase 9 Mus musculus 60-69 31489534-5 2019 Co-administration of cup and YM155 (cuYM) accelerated the intrinsic apoptosis of mature OLGs (MOG positive cells) through the upregulation of caspase-9 and caspase-3. YM 155 29-34 caspase 9 Mus musculus 142-151 31615091-3 2019 2HF induced apoptosis and inhibited the growthof the human SK-MEL-24 as well as murine B16-F0 and B16-F10 melanoma cell lines in vitro.Apoptosis was associated with depletion of caspase-3, caspase-9, and PARP1 in B16-F0 and SKMEL-24 cells. 2'-hydroxyflavanone 0-3 caspase 9 Mus musculus 189-198 31632159-6 2019 The expression of caspase-3 and caspase-9, reactive oxygen species, and the number of TUNEL-positive cells increased in the skin of irinotecan-treated mice but were lowered by high-dose vitamin C administration. irinotecan 132-142 caspase 9 Mus musculus 32-41 31632159-6 2019 The expression of caspase-3 and caspase-9, reactive oxygen species, and the number of TUNEL-positive cells increased in the skin of irinotecan-treated mice but were lowered by high-dose vitamin C administration. Ascorbic Acid 186-195 caspase 9 Mus musculus 32-41 31131920-6 2019 Increased lipid peroxidation, ROS, apoptosis, caspase-3 and caspase-9 activities in the kidney and testes of the DTX group were diminished by treatment with MEL and Se. Melatonin 157-160 caspase 9 Mus musculus 60-69 31131920-8 2019 In conclusion, our data show that MEL and Se can act as modulators against DTX-induced apoptosis and oxidative damage in the kidney and testis through up-regulation of glutathione and vitamin E and down-regulation of caspase pathways. Docetaxel 75-78 caspase 9 Mus musculus 217-224 31326607-3 2019 ROS-mediated apoptosis was accompanied by the induction of the endoplasmic reticulum (ER) stress-mediated apoptotic pathway, involving CHOP/GADD153 upregulation, JNK and p38 MAPK activation, and caspase-12 and caspase-8 activation, and subsequent induction of the mitochondrial apoptotic pathway through BAK and BAX activation, mitochondrial membrane potential (Deltapsim) loss, caspase-9 and caspase-3 activation, PARP cleavage, and nucleosomal DNA fragmentation. Reactive Oxygen Species 0-3 caspase 9 Mus musculus 379-388 31332890-5 2019 Pretreatment with BHB upregulated the level of tumor necrosis factor alpha and interleukin-6 in plasma, promoted the activities of caspase-3, caspase-8, and caspase-9 and increased the count of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. 3-Hydroxybutyric Acid 18-21 caspase 9 Mus musculus 157-166 31201698-7 2019 BPA reduced the transcriptional level of testicular DNA methyltransferase (Dnmt), increased the expression of testicular caspase-7, caspase-9, and bax, and decreased the expression of bcl-2 in F1 mice at PND 56. bisphenol A 0-3 caspase 9 Mus musculus 132-141 31197678-0 2019 Mitochondrial oxidative stress-induced brain and hippocampus apoptosis decrease through modulation of caspase activity, Ca2+ influx and inflammatory cytokine molecular pathways in the docetaxel-treated mice by melatonin and selenium treatments. Docetaxel 184-193 caspase 9 Mus musculus 102-109 31197678-0 2019 Mitochondrial oxidative stress-induced brain and hippocampus apoptosis decrease through modulation of caspase activity, Ca2+ influx and inflammatory cytokine molecular pathways in the docetaxel-treated mice by melatonin and selenium treatments. Melatonin 210-219 caspase 9 Mus musculus 102-109 31217391-5 2019 It decreased MI/R-induced activation of caspase 9, the indicator of the intrinsic mitochondrial pathway, but not caspase 8. Arginine 16-17 caspase 9 Mus musculus 40-49 30940514-10 2019 Smoothened agonist (SAG), an agonist of SHH signaling, reduced apoptosis in GANT61-treated HT22 cells by regulating caspase-9 and caspase-3 activation. sagopilone 20-23 caspase 9 Mus musculus 116-125 31316052-12 2019 In addition, our work shows that propofol-induced apoptotic initiator caspase (caspase-9) subsequently cleaved effector caspases (caspase-3 and 7), indicating that both apoptotic and pyroptotic cellular death pathways are activated after propofol exposure. Propofol 33-41 caspase 9 Mus musculus 79-88 31316052-12 2019 In addition, our work shows that propofol-induced apoptotic initiator caspase (caspase-9) subsequently cleaved effector caspases (caspase-3 and 7), indicating that both apoptotic and pyroptotic cellular death pathways are activated after propofol exposure. Propofol 238-246 caspase 9 Mus musculus 79-88 31196352-9 2019 Compared with the control group, the levels of caspase 9 and caspase 3 protein expressions were increased significantly in Tf-P-DOX group. Doxorubicin 128-131 caspase 9 Mus musculus 47-56 31030092-7 2019 In addition, pre-treatment with DEX down-regulated the expression of cleavage of caspase-3, decreased the activities of caspase-3, caspase-8, caspase-9, and consequently, reduced hepatocyte apoptosis. Dexmedetomidine 32-35 caspase 9 Mus musculus 142-151 30902848-4 2019 Emerging evidence suggests that therapeutics designed for cancer chemotherapy or inflammatory disorders such as SMAC mimetics, TAK1 inhibitors and BH3 mimetics promote caspase-8 or caspase-9-dependent inflammatory cell death and NLRP3 inflammasome activation. BH 3 147-150 caspase 9 Mus musculus 181-190 31104354-8 2019 Metallothionein transgene reversed L-NAME-induced changes in Bax, Bcl-2, BAD phosphorylation, Caspase 9, Caspase 12 and cleaved Caspase 3. NG-Nitroarginine Methyl Ester 35-41 caspase 9 Mus musculus 94-103 30942960-10 2019 Also, MOR-treated GMSCs influenced the apoptotic pathway, by reducing Bax, caspase 3, and caspase 9 expressions. moringin 6-9 caspase 9 Mus musculus 90-99 30942960-10 2019 Also, MOR-treated GMSCs influenced the apoptotic pathway, by reducing Bax, caspase 3, and caspase 9 expressions. gmscs 18-23 caspase 9 Mus musculus 90-99 31296984-8 2019 In addition, TP markedly induced apoptosis in MLTC-1 cells via increasing the expressions of Bax, active caspase 3, Cyto c and active caspase 9, and decreasing the level of Bcl-2. triptolide 13-15 caspase 9 Mus musculus 134-143 30698892-5 2019 Detailed investigation of regulatory mechanisms revealed that OTA mediated apoptosis and embryotoxicity through ROS generation, loss of mitochondrial membrane potential (MMP), and activation of caspase-9 and caspase-3, which were effectively prevented by LQ. liquiritigenin 255-257 caspase 9 Mus musculus 194-203 30246249-6 2019 Mechanistic studies showed that increased ROS levels in cells incubated with 20 muM curcumin induced opening of mitochondrial permeability transition pores and subsequent release of cytochrome c, activation of caspases 9 and 3/7, and apoptotic cell death. Reactive Oxygen Species 42-45 caspase 9 Mus musculus 210-226 30771091-7 2019 At the molecular level, suramin treatment repressed mitochondrial oxidative stress, sustained mitochondrial dynamics and blocked the caspase-9-mediated mitochondrial apoptosis pathway; these effects of suramin were achieved by reversing Mst1 expression. Suramin 24-31 caspase 9 Mus musculus 133-142 30771091-7 2019 At the molecular level, suramin treatment repressed mitochondrial oxidative stress, sustained mitochondrial dynamics and blocked the caspase-9-mediated mitochondrial apoptosis pathway; these effects of suramin were achieved by reversing Mst1 expression. Suramin 202-209 caspase 9 Mus musculus 133-142 30793867-7 2019 Furthermore, oligonol reduced expression of released cytochrome c and cleaved caspase-9 in skeletal muscle of SAMP8 mice. oligonol 13-21 caspase 9 Mus musculus 78-87 31024851-6 2019 Furthermore, the combination of MPT0G413 and BTZ enhanced polyubiquitinated protein accumulation and synergistically reduced MM viability, increased caspase-3, caspase-8, caspase-9 levels, and cleaved poly (ADP) ribosome polymerase and also inhibited adherence of MM cells to bone marrow stromal cells (BMSC) and reduced VEGF and IL-6 levels and cell growth in a co-culture system. Bortezomib 45-48 caspase 9 Mus musculus 171-180 29991712-14 2019 GLE suppressed MPP+-induced cytochrome C release and activation of caspase-3 and caspase-9. GLE 0-3 caspase 9 Mus musculus 81-90 29991712-14 2019 GLE suppressed MPP+-induced cytochrome C release and activation of caspase-3 and caspase-9. mangion-purified polysaccharide (Candida albicans) 15-19 caspase 9 Mus musculus 81-90 30520250-7 2019 However, phytol treatment reduced the expression of Bax, caspase-3, and caspase-9 protein and maintained the constant expression of anti-apoptotic protein Bcl-2. Phytol 9-15 caspase 9 Mus musculus 72-81 31081109-10 2019 In addition, Dex administration further increased the expression of MCT1, whereas decreased the expressions of cytochrome c, cleaved caspase-9 and -3 in contrast to the I/R group. Dexmedetomidine 13-16 caspase 9 Mus musculus 133-149 30601695-5 2019 Our data indicated that lunasin attenuated H2O2-induced, mitochondria-dependent endothelial apoptosis via down-regulating Bax and up-regulating Bcl-2, inhibiting the mitochondrial depolarization, and reducing the release of cytochrome c, as well as decreasing the activation of caspase-9 and caspase-3 in vitro and in vivo. Hydrogen Peroxide 43-47 caspase 9 Mus musculus 278-287 30246249-6 2019 Mechanistic studies showed that increased ROS levels in cells incubated with 20 muM curcumin induced opening of mitochondrial permeability transition pores and subsequent release of cytochrome c, activation of caspases 9 and 3/7, and apoptotic cell death. Curcumin 84-92 caspase 9 Mus musculus 210-226 30856162-13 2019 Moreover, dexmedetomidine ameliorated the altered activity of caspase-3, caspase-8, and caspase-9 enzyme in the lung tissues of CLP-induced lung injure mice. Dexmedetomidine 10-25 caspase 9 Mus musculus 88-97 30583225-9 2019 Our results also showed decreased levels of phase I enzymes (Cyt P450 and-Cyt b5) with increased levels of phase II enzymes (GR, GST and GSH) and increased expression of Bax, caspase-3 and caspase-9 with decreased expression of mutated p53 and Bcl-2 in animals treated with DMBA and D-carvone at 20 mg dose. 6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene 274-278 caspase 9 Mus musculus 189-198 30583225-9 2019 Our results also showed decreased levels of phase I enzymes (Cyt P450 and-Cyt b5) with increased levels of phase II enzymes (GR, GST and GSH) and increased expression of Bax, caspase-3 and caspase-9 with decreased expression of mutated p53 and Bcl-2 in animals treated with DMBA and D-carvone at 20 mg dose. carvone 283-292 caspase 9 Mus musculus 189-198 30218457-4 2019 Additionally, the accumulation of ROS caused mitochondrial dysfunction, leading to the activation of caspase-9 and -3, thereby resulting in apoptosis. Reactive Oxygen Species 34-37 caspase 9 Mus musculus 101-117 30602716-0 2019 Selenium-Rich Diet Induces Myocardial Structural and Functional Abnormalities by Activating Caspase-9 and Caspase-3 in Gpx-1P198L-Overexpression Transgenic Mice. Selenium 0-8 caspase 9 Mus musculus 92-101 30657151-6 2019 CGA significantly inhibited Pb-induced increase of cytoplasmic NF-kappaB, Bax, cytochrome C, and caspase-9 protein expressions. Chlorogenic Acid 0-3 caspase 9 Mus musculus 97-106 30657151-6 2019 CGA significantly inhibited Pb-induced increase of cytoplasmic NF-kappaB, Bax, cytochrome C, and caspase-9 protein expressions. Lead 28-30 caspase 9 Mus musculus 97-106 30833897-5 2019 GLA downregulated pro-apoptotic proteins (Bax, cleaved-caspase 9 and cleaved-caspase 3) and upregulated anti-apoptotic proteins (HAX-1 and Bcl-2) in the cardiac tissues. glabridin 0-3 caspase 9 Mus musculus 55-64 30537677-15 2019 Knockdown of GSK3beta alleviated Dex-induced osteoblast and MC3T3-E1 cell apoptosis by decreasing the expressions of Bax, cleaved-caspase 3, cleaved-caspase 9 and increasing the expression of Bcl-2. Dexamethasone 33-36 caspase 9 Mus musculus 149-158 30697271-9 2019 Moreover, THSG was identified to reverse the elevation of caspase-3, caspase-9 and Bax and the reduction of Bcl-2 induced by H2O2. thsg 10-14 caspase 9 Mus musculus 69-78 29804319-9 2019 Furthermore, upregulation of miR-219 inhibits positive expression of Bax, caspase-9, and caspase-3 proteins, leading to the suppression of hippocampal neuronal cell apoptosis. mir-219 29-36 caspase 9 Mus musculus 74-83 31530262-7 2019 In addition, in GA muscle of the mice fed with DDC-supplemented diet-induced CLD showed increased myonuclear apoptosis compared with the GA muscle of the control diet-fed mice, as evidenced by increased apoptotic nuclei number, caspase-8 and caspase-9 expression, enzymatic activity of caspase-3 and BAX/BCL-2 ratio. Zalcitabine 47-50 caspase 9 Mus musculus 242-251 30745820-11 2019 Furthermore, ICA significantly inhibited the expression of ER stress apoptotic proteins caspase-12, CHOP, Bax/Bcl-2, caspase-9 and caspase-3. icariin 13-16 caspase 9 Mus musculus 117-126 31679311-4 2019 With respect to apoptosis, fucoxanthin treated animals shows increased apoptosis compared to tumor induced mice by increased expression of caspase 9 and 3 and decreased expression of anti-apoptotic Bcl2 protein. fucoxanthin 27-38 caspase 9 Mus musculus 139-154 30602716-14 2019 Se supplementation significantly reduced pathological changes, as well as caspase-9 and caspase-3 levels in the presence of increased myocardial fibrosis. Selenium 0-2 caspase 9 Mus musculus 74-83 30602716-16 2019 In Se-supplemented Tg mice, myocardial fibrosis and caspase-9 level were increased, although pathological injuries and caspase-3 were similar to that in Se-supplemented WT mice. Selenium 3-5 caspase 9 Mus musculus 52-61 30241048-8 2018 Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC). cadmium nitrate 13-21 caspase 9 Mus musculus 41-49 30315841-8 2019 Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies. Acetylcysteine 15-18 caspase 9 Mus musculus 99-108 30594149-4 2018 RESULTS: CoCl2 caused cell death in a dose-dependent manner and increased protein levels of cleaved caspase-9 and caspase-3. cobaltous chloride 9-14 caspase 9 Mus musculus 100-109 30594149-5 2018 Rapamycin increased viability of HT22 cells exposed to CoCl2 and reduced activation of caspases-9 and -3. Sirolimus 0-9 caspase 9 Mus musculus 87-104 30594149-13 2018 Additionally, inhibition of caspase-9 and -3 activation and stimulation of protective autophagy reduces cell death, while a decrease in the Bax/Bcl-2 ratio and an increase in pMAPK promotes cell survival during CoCl2 exposure. cobaltous chloride 211-216 caspase 9 Mus musculus 28-44 30587838-6 2018 High glucose triggered cell apoptosis via the the loss of mitochondrial membrane potential, depletion of adenosine triphosphate, upregulation of caspases 9 and 3, enhancement of cytochrome c release, and subsequent interruption of the Bax/Bcl-2 balance. Glucose 5-12 caspase 9 Mus musculus 145-161 30573978-8 2018 Additionally, the results also showed that ERK1/2 agonist (EGF) or a caspase 3 inhibitor (Z-DEVD-FMK) inhibited activity of caspase 3 and caspase 9 and cell apoptosis rate. benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone 90-100 caspase 9 Mus musculus 138-147 30564112-11 2018 In addition, NaIO3-induced retinal damage was related to apoptosis via caspase 8 and caspase 9, but not the caspase 3 pathways, which led to upregulation of Bax and p53, downregulation of Bcl-2, and increase in Jc-1-positive cells in mice. sodium iodate 13-18 caspase 9 Mus musculus 85-94 30241048-8 2018 Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC). Acetylcysteine 124-143 caspase 9 Mus musculus 41-49 30241048-8 2018 Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC). Acetylcysteine 145-148 caspase 9 Mus musculus 41-49 30241048-9 2018 These results indicated that Cd(NO3)2-induced neuronal apoptosis was reduced by NAC via intrinsic apoptotic caspase cascade activities and their up-stream factors, including mitochondrial dysfunction and ROS generation. cadmium nitrate 29-37 caspase 9 Mus musculus 108-115 30241048-9 2018 These results indicated that Cd(NO3)2-induced neuronal apoptosis was reduced by NAC via intrinsic apoptotic caspase cascade activities and their up-stream factors, including mitochondrial dysfunction and ROS generation. Acetylcysteine 80-83 caspase 9 Mus musculus 108-115 30312649-7 2018 Both caspase-dependent, including caspase-9, caspase-3, and PARP-1 cleavage, and caspase-independent, such as nuclear translocation of AIF, pathways were activated by BPA. bisphenol A 167-170 caspase 9 Mus musculus 34-43 30342188-8 2018 The level of caspase-9 and caspase-3, upregulated following GD, were reduced by treatment with RSV. Resveratrol 95-98 caspase 9 Mus musculus 13-22 30469321-5 2018 Western blotting showed that PDQ reversed the CDDP-induced (1) downregulation of Sirtuin-1 (Sirt-1), nuclear-related factor 2 (Nrf2), and Bcl-2, and (2) upregulation of NF-kappaB, Nox-4, Bax, caspase-9, and caspase-3. Cisplatin 46-50 caspase 9 Mus musculus 192-201 30310905-5 2018 EGCG induced breast cancer apoptotic cell death at 24 h, as evidenced by annexin V/PI, caspase 3, caspase 8 and caspase 9 activation. epigallocatechin gallate 0-4 caspase 9 Mus musculus 112-121 30533172-10 2018 Coherently, apoptotic gene expressions (Casp3, Casp9, Bax, and Parp8) were significantly increased in the retina with increasing dosages of H2O2, while Bcl2 expression was mildly decreased. Hydrogen Peroxide 140-144 caspase 9 Mus musculus 47-52 30134043-5 2018 Cav-1 deletion significantly reduced LPS/GalN-induced caspase-3, caspase-8 and caspase-9 activation and pro-inflammatory cytokine and chemokine expression. Galactosamine 41-45 caspase 9 Mus musculus 79-88 30241783-8 2018 The protective effects of PPX patch was also associated with downregulation of the Bax/Bcl-2 ratio and Apaf-1, inhibition of cytochrome c release and inactivation of caspase-9 and caspase-3. paclitaxel poliglumex 26-29 caspase 9 Mus musculus 166-175 30314494-9 2018 CTPG treatment significantly increased Bax/Bcl-2 ratio, reduced Deltapsim and enhanced the release of cytochrome c. The levels of cleaved caspase-8 and caspase-9 in both extrinsic and intrinsic signaling pathways were significantly increased that sequentially activated caspase-7 and -3 to cleave PARP. ctpg 0-4 caspase 9 Mus musculus 152-161 30310156-6 2018 In addition, P53, gammaH2AX, caspase8, caspase9 and caspase3 expression were all reduced by TQ. thymoquinone 92-94 caspase 9 Mus musculus 39-47 29594946-5 2018 Simultaneously, compared with the control group, the expression levels of Bax, Bcl-2, Cyt c, caspase-3, and caspase-9 were up-regulated after fluoride treatment. Fluorides 142-150 caspase 9 Mus musculus 108-117 29594946-6 2018 Excessive fluoride damages the ultrastructure in mitochondria, leading to the release of Cyt c from the mitochondria to cytoplasm in C2C12 cells; thereby, activated caspases cascade apoptosis process through a mitochondria-mediated pathway. Fluorides 10-18 caspase 9 Mus musculus 165-173 30568691-5 2018 The effect of PEITC on caspase-9 enzyme activity was also tested. phenethyl isothiocyanate 14-19 caspase 9 Mus musculus 23-32 30568691-9 2018 Bax, caspase-9 genes" expression and caspase-9 enzymatic activity were significantly increased, while Bcl-2 gene expression was significantly decreased in PEITC treated mice. phenethyl isothiocyanate 155-160 caspase 9 Mus musculus 5-14 30303271-9 2018 The effect of chlorophyllin on apoptosis showed the downregulation of cysteine-dependent aspartate-specific protease (caspase) 3 and caspase 9, whereas upregulation of B-cell lymphoma-2 (Bcl-2) protein, and the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) assay demonstrated a few apoptotic cells. chlorophyllin 14-27 caspase 9 Mus musculus 133-142 29802833-6 2018 In addition, qRT-PCR and western blot demonstrated that downstream substrates of apoptotic and TNF signaling pathways, caspase-9, MAP3K and JNK, were all significantly downregulated by TNF-alpha or TNF-R1 inhibition, but not by TNF-R2 inhibition, in bupivacaine-injured DRG. Bupivacaine 250-261 caspase 9 Mus musculus 119-128 30116378-6 2018 Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H2O2. Hydrogen Peroxide 216-220 caspase 9 Mus musculus 176-185 29894864-5 2018 Treatment with DA also suppressed LPS/D-Gal-induced production of TNF-alpha, phosphorylation of c-jun-N-terminal kinase (JNK), cleavage of caspase-3, up-regulation of hepatic caspase-3, caspase-8, and caspase-9 activities and reduced the count of TUNEL-positive hepatocytes. Dopamine 15-17 caspase 9 Mus musculus 201-210 29894864-5 2018 Treatment with DA also suppressed LPS/D-Gal-induced production of TNF-alpha, phosphorylation of c-jun-N-terminal kinase (JNK), cleavage of caspase-3, up-regulation of hepatic caspase-3, caspase-8, and caspase-9 activities and reduced the count of TUNEL-positive hepatocytes. Deuterium 15-16 caspase 9 Mus musculus 201-210 29894864-5 2018 Treatment with DA also suppressed LPS/D-Gal-induced production of TNF-alpha, phosphorylation of c-jun-N-terminal kinase (JNK), cleavage of caspase-3, up-regulation of hepatic caspase-3, caspase-8, and caspase-9 activities and reduced the count of TUNEL-positive hepatocytes. cyclohexenoesculetin-beta-galactoside 40-43 caspase 9 Mus musculus 201-210 29752567-10 2018 Moreover, in bupivacaine-injured DRG, EZH2 downregulation reduced caspase-9, whereas upregulated TrkC and phosphorylated-TrkC (p-TrkC). Bupivacaine 13-24 caspase 9 Mus musculus 66-75 29442721-8 2018 Additionally, real-time PCR data analysis shown an increased in the expression of p53, Bax, caspase-9, caspase-3 and decreased the level of Bcl-2, by this means specifying that apoptosis induced by TiO2 NPs occurs via the caspase-dependent pathway. titanium dioxide 198-202 caspase 9 Mus musculus 92-101 30066945-6 2018 The western blot analysis revealed that N2a cells treated with etomidate had a significant modulation of pro-apoptotic proteins, includingpoly ADP-ribose polymerase (PARP), cleaved PARP, caspase-9 and procaspase-3. Etomidate 63-72 caspase 9 Mus musculus 187-196 29565730-0 2018 Acetyl-macrocalin B, an ent-kaurane diterpenoid, initiates apoptosis through the ROS-p38-caspase 9-dependent pathway and induces G2/M phase arrest via the Chk1/2-Cdc25C-Cdc2/cyclin B axis in non-small cell lung cancer. macrocalin B 6-19 caspase 9 Mus musculus 89-98 29448197-7 2018 Furthermore, the expression of mRNA in PI3K, BAD, Bcl-2, Bax and caspase-9 were significantly increased in the fluoride group (P < 0.01), while the expression of PDK1 was markedly decreased (P < 0.01). Fluorides 111-119 caspase 9 Mus musculus 65-74 29867489-10 2018 Mechanistically, EAEO significantly decreased the ratio of Bcl-2/Bax and resulted in the activation of caspase-9 and -3. eaeo 17-21 caspase 9 Mus musculus 103-119 29616245-8 2018 Furthermore, THC substantially induced the release of cytochrome C, caspase-3, caspase-9 and the cleavage of PARP to induce H22 cell apoptosis. Dronabinol 13-16 caspase 9 Mus musculus 79-88 29670107-6 2018 Mechanistic studies reveal that Z-DAN-11 induces the expression of pro-apoptotic proteins and decreases anti-apoptotic protein expression that decisively helps in the activation of caspase 8, caspase 9, and caspase 3, leading to cleavage of PARP1 and cell death via intrinsic and extrinsic pathways of apoptosis. z-dan-11 32-40 caspase 9 Mus musculus 192-201 29512789-7 2018 Tetrahydropalmatine also suppressed iNOS protein expression, weakened caspase-3 and caspase-9 activation, inhibited nuclear factor-kappaB, glial fibrillary acidic protein, cytochrome c and phospholipase C-gamma1 protein expression, and induced glial cell-derived neurotrophic factor protein expression in ketamine-induced mice. tetrahydropalmatine 0-19 caspase 9 Mus musculus 84-93 29568940-10 2018 The data indicated that apoptosis-associated genes, including caspase-3, BCL2 associated X, BH3 interacting domain death agonist and caspase-9, were downregulated in hippocampal cells isolated from nicergoline-treated experimental mice. Nicergoline 198-209 caspase 9 Mus musculus 133-142 28357806-2 2018 Our study demonstrated that BP-3 caused neurotoxicity and activated apoptosis via an intrinsic pathway involving the loss of mitochondrial membrane potential and the activation of caspases-9 and -3 and kinases p38/MAPK and Gsk3beta. oxybenzone 28-32 caspase 9 Mus musculus 180-197 29432840-6 2018 Conversely, pre-treatment of the cells with the Nrf2 inhibitor brusatol or the HO-1 inhibitor zinc protoporphyrin IX, enhanced T-2 toxin induced neurotoxicity and increased the activation of caspase-9 and -3. brusatol 63-71 caspase 9 Mus musculus 191-207 29432840-6 2018 Conversely, pre-treatment of the cells with the Nrf2 inhibitor brusatol or the HO-1 inhibitor zinc protoporphyrin IX, enhanced T-2 toxin induced neurotoxicity and increased the activation of caspase-9 and -3. zinc protoporphyrin 94-116 caspase 9 Mus musculus 191-207 29308536-10 2018 The apoptosis induced by Rabd-B could be partially reversed by a caspase-9-specific inhibitor (Z-LEHD-FMK) and a pan-caspase inhibitor (Z-VAD-FMK). benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 95-105 caspase 9 Mus musculus 65-74 29630131-9 2018 Butorphanol reduced the myocardial infarct size, serum CTn I and CK-MB levels, expression of cleaved caspase-9 and -3, and phosphorylation levels of p38 and JNK (all p < 0.01). Butorphanol 0-11 caspase 9 Mus musculus 101-117 29328461-6 2018 The tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and IL-18 concentrations, and caspase-3 and caspase-9 were significantly inhibited by gambogic acid in arthritic mice. gambogic acid 154-167 caspase 9 Mus musculus 112-121 29328487-7 2018 We determined that the combination of gemcitabine and erlotinib inhibited recurrent tumor growth and induced apoptosis in vivo by downregulating phosphorylation levels of JAKs and STATs, which in turn downregulated the downstream proteins HIF-1alpha and cyclin D1, and upregulated caspase-9 and caspase-3 expression. gemcitabine 38-49 caspase 9 Mus musculus 281-290 29328487-7 2018 We determined that the combination of gemcitabine and erlotinib inhibited recurrent tumor growth and induced apoptosis in vivo by downregulating phosphorylation levels of JAKs and STATs, which in turn downregulated the downstream proteins HIF-1alpha and cyclin D1, and upregulated caspase-9 and caspase-3 expression. Erlotinib Hydrochloride 54-63 caspase 9 Mus musculus 281-290 29467906-6 2018 Additionally, beta-elemene-ligustrazine caused a decrease in nuclear factor-kappaB, interleukin-8, C-X-C motif chemokine receptor 4 and urokinase-type plasminogen activator mRNA expression, as well as an increase in caspase-3, caspase-8, and caspase-9 mRNA expression. beta-elemene-ligustrazine 14-39 caspase 9 Mus musculus 242-251 29403554-10 2018 Mechanism analysis demonstrated that berberine inhibited apoptotic protease-activating factor 1, caspase-3 and caspase-9 expression in myocardial cells. Berberine 37-46 caspase 9 Mus musculus 111-120 29289836-6 2018 Cleaved-caspase-8, cleaved-caspase-9 and cleaved-caspase-3 were up-regulated after Brevilin A treatment, together with an increase of Bax protein expression, while Bcl-2 was reduced. brevilin A 83-93 caspase 9 Mus musculus 27-36 29174113-10 2018 Rotenone decreased the protein levels of Bcl-2 and increased the protein levels of Bax, cleaved caspase-3 and cleaved caspase-9, and this effect was reversed by ghrelin treatment. Rotenone 0-8 caspase 9 Mus musculus 118-127 29174113-10 2018 Rotenone decreased the protein levels of Bcl-2 and increased the protein levels of Bax, cleaved caspase-3 and cleaved caspase-9, and this effect was reversed by ghrelin treatment. Ghrelin 161-168 caspase 9 Mus musculus 118-127 29441017-14 2018 DHTS increased the expression of several apoptosis-related proteins, including caspase9, caspase3, PARP, AIF, BAX, cytochrome c, caspase8 and FADD and significantly inhibited angiogenesis, as indicated by reduced tube formation and diminished expression of vascular endothelial cell growth factor receptor 2 and matrix metalloproteinase 9. dhts 0-4 caspase 9 Mus musculus 79-87 29351226-4 2018 Curcumin pre-treatment at 50, 100 and 200 mg/kg significantly ameliorated CCl4-induced oxidative stress, characterized by decreased malondialdehyde (MDA) formations, and increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) content, followed by a decrease in caspase-9 and -3 activities. Curcumin 0-8 caspase 9 Mus musculus 291-307 29254330-7 2018 A further mechanistic study revealed that the protective effect of DHA-PC on vancomycin-mediated toxicity might be attributed to its ability to inhibit oxidative stress and inactivate mitogen-activated protein kinase (MAPK) signaling pathways, which was associated with upregulation of Bcl-2 and downregulation of caspase-9, caspase-3, cytochrome-c, p38, and JNK. dha-pc 67-73 caspase 9 Mus musculus 314-323 29254330-7 2018 A further mechanistic study revealed that the protective effect of DHA-PC on vancomycin-mediated toxicity might be attributed to its ability to inhibit oxidative stress and inactivate mitogen-activated protein kinase (MAPK) signaling pathways, which was associated with upregulation of Bcl-2 and downregulation of caspase-9, caspase-3, cytochrome-c, p38, and JNK. Vancomycin 77-87 caspase 9 Mus musculus 314-323 30043652-4 2018 Action mechanism studies manifested that DQA modified paclitaxel plus honokiol micelles could activate apoptotic enzymes caspase-3 and caspase-9 as well as down-regulate FAK, PI3K, MMP-2 and MMP-9. Paclitaxel 54-64 caspase 9 Mus musculus 135-144 30043652-4 2018 Action mechanism studies manifested that DQA modified paclitaxel plus honokiol micelles could activate apoptotic enzymes caspase-3 and caspase-9 as well as down-regulate FAK, PI3K, MMP-2 and MMP-9. honokiol 70-78 caspase 9 Mus musculus 135-144 29207476-10 2017 Hesperidin inhibited high glucose-induced cell apoptosis by attenuating the downregulation of caspase-9, caspase-3, and Bax/Bcl-2. Hesperidin 0-10 caspase 9 Mus musculus 94-103 29929190-15 2018 TUNEL staining, caspase-3, and caspase-9 activity assays consistently revealed that alcohol-induced microglial apoptosis was inhibited by depletion of p65. Alcohols 84-91 caspase 9 Mus musculus 31-40 28636115-8 2018 Decreased survival rates and cleaved PARP expression, increased cell apoptosis rate,expressions of caspase 3 and caspase 9 in Hca-F and Hca-P cells were detected in groups that had been cultured in a medium containing octreotide. Octreotide 218-228 caspase 9 Mus musculus 113-122 29490300-12 2018 Furthermore, PA treatment induced mitochondrial impairment, and triggered the release of cytochrome c from the mitochondria to cytosol, with a concomitant dose-dependent increase in the levels of cleaved caspase-9, cleaved caspase-3, and PARP. Palmitic Acid 13-15 caspase 9 Mus musculus 204-213 28822080-9 2018 attenuated MPTP-induced reduction in striatal dopamine content, TH-positive cell numbers, TH, and pro-caspase 9 protein levels (an initiator caspase of apoptosis) in mouse SN. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 11-15 caspase 9 Mus musculus 102-111 29115645-7 2018 In addition, apoptosis induced by 3-BrPA and SCT was initiated by the upregulation of Bax and downregulation of Bcl-2, which promote cytochrome c release and subsequently activate caspase-9 and -3, and ultimately execute mitochondria-mediated apoptosis. bromopyruvate 34-40 caspase 9 Mus musculus 180-196 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. z-le(ome 76-84 caspase 9 Mus musculus 56-65 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. z-le(ome 76-84 caspase 9 Mus musculus 309-318 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. (ome)-fluoromethylketone 87-111 caspase 9 Mus musculus 56-65 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. (ome)-fluoromethylketone 87-111 caspase 9 Mus musculus 309-318 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. FMK 112-115 caspase 9 Mus musculus 56-65 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. FMK 112-115 caspase 9 Mus musculus 309-318 29241307-7 2017 Further studiesshowed that intravenous injection of the caspase-9 inhibitor Z-LE(OMe)HD(OMe)-fluoromethylketone(FMK) into the mice could significantly inhibit apoptosis of the platelets and the effect of CSAtreatment when compared to the BMF group, and exerted a better protective effect from apoptosis ifthe caspase-9 inhibitor was combined with the CSA treatment. Cyclosporine 204-207 caspase 9 Mus musculus 56-65 29312001-5 2017 Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. Cisplatin 15-24 caspase 9 Mus musculus 82-90 29312001-5 2017 Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. Cisplatin 15-24 caspase 9 Mus musculus 100-108 29416617-6 2018 Pretreatment of DOX-treated mice with LDR also decreased DOX-induced cardiac cell apoptosis (TUNEL staining and cleaved caspase-3) and mitochondrial apoptotic pathway (increased p53, Bax, and caspase-9 expression and decreased Bcl2 expression and DeltaPsim dissipation). Doxorubicin 16-19 caspase 9 Mus musculus 192-201 29416617-6 2018 Pretreatment of DOX-treated mice with LDR also decreased DOX-induced cardiac cell apoptosis (TUNEL staining and cleaved caspase-3) and mitochondrial apoptotic pathway (increased p53, Bax, and caspase-9 expression and decreased Bcl2 expression and DeltaPsim dissipation). Doxorubicin 57-60 caspase 9 Mus musculus 192-201 29207476-10 2017 Hesperidin inhibited high glucose-induced cell apoptosis by attenuating the downregulation of caspase-9, caspase-3, and Bax/Bcl-2. Glucose 26-33 caspase 9 Mus musculus 94-103 29312803-4 2017 Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway. Sorafenib 16-25 caspase 9 Mus musculus 154-162 29174851-7 2017 The expression of Bax, Bcl-2, Beclin-1, LC3, P62 and caspase 9 were markedly affected by quercetin pretreatment. Quercetin 89-98 caspase 9 Mus musculus 53-62 29312803-4 2017 Co-treatment of sorafenib and VPA synergistically inhibited HCC cell viability, induced cell apoptosis, along with the up-regulation of p21, Bax, cleaved caspase9, cleaved caspase3, cleaved PARP and down-regulation of Bcl-xL, suggesting this combination activated intrinsic apoptotic pathway. Valproic Acid 30-33 caspase 9 Mus musculus 154-162 29053994-6 2017 Caspase-9, -8 and -3 activities were elevated significantly (P<.05) in myoblasts treated with H2O2. Hydrogen Peroxide 97-101 caspase 9 Mus musculus 0-20 29053994-9 2017 Resveratrol reduced the apoptotic index and significantly reduced the ROS-induced caspase-9, -8 and -3 activity in myoblasts. Resveratrol 0-11 caspase 9 Mus musculus 82-102 29053994-9 2017 Resveratrol reduced the apoptotic index and significantly reduced the ROS-induced caspase-9, -8 and -3 activity in myoblasts. Reactive Oxygen Species 70-73 caspase 9 Mus musculus 82-102 29171326-10 2017 By treating with EDN (10, 20 and 40 muM), expression of caspase-3, caspase-9, Bax, P53 and phosphorylated JNK in A549 cells were significantly upregulated, whereas expression of Bcl-2 and Akt phosphorylation were significantly down-regulated. eudesmin 17-20 caspase 9 Mus musculus 67-76 29179722-10 2017 The caspase-9 and caspase-3 cascade was activated by the AG-PEG-SS-PLA/PTX nanomicelles through upregulation of the pro-apoptotic proteins Bax and Bid and suppression of the anti-apoptotic protein Bcl-2, thereby increasing apoptosis. Paclitaxel 71-74 caspase 9 Mus musculus 4-13 29186930-7 2017 CTN-induced damage processes directly promoted reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (MMP) and activation of caspase-9 and caspase-3, which were effectively blocked by LQ. Citrinin 0-3 caspase 9 Mus musculus 154-163 29186930-7 2017 CTN-induced damage processes directly promoted reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (MMP) and activation of caspase-9 and caspase-3, which were effectively blocked by LQ. liquiritigenin 213-215 caspase 9 Mus musculus 154-163 28900799-6 2017 The mRNA expressions of Caspase-8, Caspase-9, Apaf1, and Bax were increased and, meanwhile, the mRNA expression of Bcl-2 was decreased in response to ONOO- treatment. onoo 150-154 caspase 9 Mus musculus 35-44 29072704-8 2017 Instead, inhibition of Caspase-8 shifted the ethanol-induced death signals towards pronounced activation of the intrinsic, mitochondria-dependent apoptosis pathway in Casp8Deltahepa livers involving enhanced release of cytochrome c, stronger Caspase-9 activation and specific morphological changes of mitochondria. Ethanol 45-52 caspase 9 Mus musculus 242-251 28766664-8 2017 THC also decreased the expression of Bcl-2 significantly and increased the expression of Bcl2-associated X, resulting in the release of cytochrome C. THC significantly activated and induced cleavage of caspase-3 and caspase-9 to induce the apoptosis of H22 cells. tetrahydrocurcumin 0-3 caspase 9 Mus musculus 216-225 28766664-8 2017 THC also decreased the expression of Bcl-2 significantly and increased the expression of Bcl2-associated X, resulting in the release of cytochrome C. THC significantly activated and induced cleavage of caspase-3 and caspase-9 to induce the apoptosis of H22 cells. tetrahydrocurcumin 150-153 caspase 9 Mus musculus 216-225 28684300-8 2017 CONCLUSION: The mechanism underlying the antitumor effects of the oral liquid formulation of Poriacocos polysaccharides involved inhibition of Bcl-2 expression and activation of caspase-9 expression in sarcoma 180 cells. Polysaccharides 104-119 caspase 9 Mus musculus 178-187 28718066-8 2017 In HT-22 cells, the apoptosis rate was significantly higher and caspase 9 activation was also significantly increased in the glutamate-induced apoptosis group compared to the L and H taurine groups. Glutamic Acid 125-134 caspase 9 Mus musculus 64-73 29110957-11 2017 In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes. CHEMBL3769558 18-21 caspase 9 Mus musculus 95-104 29110957-11 2017 In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes. Doxorubicin 49-60 caspase 9 Mus musculus 95-104 27987330-7 2017 Successively, dexmedetomidine decreased cytochrome c release from mitochondria to the cytoplasm and consequent cascade activations of caspases-9, -3, and -6 in I/R-treated neuro-2a cells. Dexmedetomidine 14-29 caspase 9 Mus musculus 134-156 28677092-10 2017 Similarly, decreasing levels of cleaved caspase-12, caspase-9, caspase-3 and increasing level of uncleaved PARP were observed in chlorogenic acid groups compared with those in the fibrosis group both in vivo and in vitro. Chlorogenic Acid 129-145 caspase 9 Mus musculus 52-61 28371286-11 2017 Our in vitro results indicate that ginsenoside Rg1 treatment increases intracellular oxidative stress, decreases mitochondrial membrane potential, increases the Bax/Bcl-2 ratio, and activates caspase-9 and caspase-3, but not caspase-8. Ginsenosides 35-46 caspase 9 Mus musculus 192-201 28831032-11 2017 Moreover, specific siRNAs of ILK, Nrf-2, and HO-1, and inhibitors of HO-1 and ILK significantly increased ROS generation and Caspase9/3 expression in the presence of salidroside and HG. rhodioloside 166-177 caspase 9 Mus musculus 125-133 28798484-5 2017 In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. epigallocatechin gallate 15-19 caspase 9 Mus musculus 133-142 28798484-5 2017 In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Hydrogen Peroxide 61-65 caspase 9 Mus musculus 133-142 29113340-6 2017 Analgecine treatments also activated apoptotic signaling with increased levels of pro-apoptotic proteins, including cytochrome c, caspase-3, cleaved caspase-3, caspase-9, p53 and Bax, and decreased Bcl2. analgecine 0-10 caspase 9 Mus musculus 160-169 28529240-9 2017 Curcumin-mediated inhibition of ROS, down-regulation of caspases, restoration of MMP, and recovery of cell viability were partially reversed by HO-1 inhibitor (SnPP). Curcumin 0-8 caspase 9 Mus musculus 56-64 28396364-7 2017 In fact, activation of several proapoptotic markers (caspase-9, caspase-3, and PARP) and reversion of the cytotoxic effect upon treatment with an apoptosis inhibitor (Z-VAD-FMK) were observed. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 167-176 caspase 9 Mus musculus 53-62 28195491-4 2017 Herein we report trichosanthin, a plant protein toxin, possesses synergistic effect with paclitaxel (PTX) in the PTX-resistance A549/T nonsmall cell lung cancer (NSCLC) cells, by reversing PTX-caused caspase 9 phosphorylation and inducing caspase 3-dependent apoptosis. Paclitaxel 89-99 caspase 9 Mus musculus 200-209 28674496-10 2017 API-induced apoptosis was sustained by the increase of Bax/Bcl-2 ratio, increase of p53 expression, activation of both caspase 9 and caspase 8, cleavage of PARP-1, and increase of the percentage of cells in subG1 phase. Apigenin 0-3 caspase 9 Mus musculus 119-128 28195491-4 2017 Herein we report trichosanthin, a plant protein toxin, possesses synergistic effect with paclitaxel (PTX) in the PTX-resistance A549/T nonsmall cell lung cancer (NSCLC) cells, by reversing PTX-caused caspase 9 phosphorylation and inducing caspase 3-dependent apoptosis. Paclitaxel 101-104 caspase 9 Mus musculus 200-209 28195491-4 2017 Herein we report trichosanthin, a plant protein toxin, possesses synergistic effect with paclitaxel (PTX) in the PTX-resistance A549/T nonsmall cell lung cancer (NSCLC) cells, by reversing PTX-caused caspase 9 phosphorylation and inducing caspase 3-dependent apoptosis. Paclitaxel 113-116 caspase 9 Mus musculus 200-209 28195491-4 2017 Herein we report trichosanthin, a plant protein toxin, possesses synergistic effect with paclitaxel (PTX) in the PTX-resistance A549/T nonsmall cell lung cancer (NSCLC) cells, by reversing PTX-caused caspase 9 phosphorylation and inducing caspase 3-dependent apoptosis. Paclitaxel 113-116 caspase 9 Mus musculus 200-209 28384256-7 2017 Probucol treatment reduced the number of cells positive for 8-hydroxyl-2"-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-kappaB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice. Probucol 0-8 caspase 9 Mus musculus 218-227 26990902-5 2017 Triptolide increased protein levels of Fas, Fas-L, Bax, cytochrome c, caspase-9, Endo G, Apaf-1, PARP, caspase-3 but reduced levels of AIF, ATF6alpha, ATF6beta, and GRP78 in WEHI-3 cells. triptolide 0-10 caspase 9 Mus musculus 70-79 28183656-6 2017 Interestingly, both Cdots and CNBs are biocompatible to normal cell lines but cytotoxic to cancer cell lines, observed during several in vitro experiments (cell viability assay, cell cycle assay, apoptosis assay, ROS determination assay, caspase-9 activity assay). cdots 20-25 caspase 9 Mus musculus 238-247 28183656-6 2017 Interestingly, both Cdots and CNBs are biocompatible to normal cell lines but cytotoxic to cancer cell lines, observed during several in vitro experiments (cell viability assay, cell cycle assay, apoptosis assay, ROS determination assay, caspase-9 activity assay). cnbs 30-34 caspase 9 Mus musculus 238-247 27940053-6 2017 Moreover, paeonol inhibited epirubicin-induced apoptosis by suppressing the activation of caspase-9 and caspase-3, the Bax/Bcl-2 imbalance and cytochrome c release. paeonol 10-17 caspase 9 Mus musculus 90-99 27998766-6 2017 Western blot showed that DON significantly increased the expression levels of apoptosis-related protein including Caspase-9, Caspase-3, poly (ADP-ribose) polymerase (PARP) and the ratio of Bax/Bcl-2. deoxynivalenol 25-28 caspase 9 Mus musculus 114-123 28103798-4 2017 RESULTS: We find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Glutamic Acid 22-31 caspase 9 Mus musculus 125-141 27940053-6 2017 Moreover, paeonol inhibited epirubicin-induced apoptosis by suppressing the activation of caspase-9 and caspase-3, the Bax/Bcl-2 imbalance and cytochrome c release. Epirubicin 28-38 caspase 9 Mus musculus 90-99 26643564-8 2017 In addition, spermatogenic dysfunction induced by busulfan gradually enhanced the apoptosis and elevated the expression of caspase 3, caspase 6, and caspase 9, but decreased the expression of caspase 7 in spermatogenic cells. Busulfan 50-58 caspase 9 Mus musculus 149-158 28849533-8 2017 The doxorubicin-induced acute kidney injury model displayed a significant increase in the renal expression of apoptosis-related proteins (p53, phospho-p53, caspase 9, and caspase 3), whereas in the taurine-treated mice, the augmented expression of renal inflammation-related mRNAs such as NF-kB, COX-2, and iNOS was down-regulated. Doxorubicin 4-15 caspase 9 Mus musculus 156-165 27634671-10 2017 GKT137831 also decreased alcohol-induced apoptosis coupled with decreased insertion of Bax into mitochondria and decreased activation of cleaved caspase-9 and cleaved PARP. Alcohols 25-32 caspase 9 Mus musculus 145-154 26643564-9 2017 However, when spermatogenic cells were mostly disappeared at the fourth week after busulfan treatment, caspase 7 expression in Leydig cells was significantly increased and positively correlated with the expression of caspase 3, caspase 6, and caspase 9. Busulfan 83-91 caspase 9 Mus musculus 243-252 27262279-6 2016 The ER stress marker of PERK, eIF2alpha, ATF4, Chop, JNK, caspase-12, caspase-9, GRP94, and Bax at the mRNA levels were higher expression in 30nm ZnO NP than that in bulk or 90nm ZnO. Zinc Oxide 146-149 caspase 9 Mus musculus 70-79 27719722-15 2016 (5) Comparing with negative control group, IFNalpha-2b combined with each dose of 13cRA significantly decreased the levels of cycling D1 and procaspase-9, while increased the level of cleaved caspase-9 (P<0.05), which were similar to the positive control group (P>0.05). Isotretinoin 82-87 caspase 9 Mus musculus 144-153 27271513-5 2016 Treatment of RAW 264.7 cells with MSU crystals induced activation of Bax, caspase-3, caspase-9, and PARP1 at the early phase, in addition to enhancing IL-1beta expression, but these findings were attenuated at the late phase. Uric Acid 34-37 caspase 9 Mus musculus 85-94 27271513-6 2016 MSU crystals induced ubiquitination of p62, followed by ubiquitination of TRAF6 and caspase-9, which were significantly reversed by ascorbic acid. Ascorbic Acid 132-145 caspase 9 Mus musculus 84-93 27271513-8 2016 The antioxidant ascorbic acid inhibited p62, caspase-9, and IL-1beta expression increased by MSU crystals. Ascorbic Acid 16-29 caspase 9 Mus musculus 45-54 26438401-9 2016 We found that KCa3.1 blockade attenuated cytochrome c release and the increase in the intrinsic apoptotic mediators Bax, Bak, and caspase-9 after cisplatin treatment. Cisplatin 146-155 caspase 9 Mus musculus 130-139 27928554-6 2016 RESULTS: Exposure to Bleo significantly induced AGT protein (p<0.02), extracellular ANGII levels (p< 0.005) and the active form of caspase-9 (p<0.05) in neonatal lung tissue. Bleomycin 21-25 caspase 9 Mus musculus 137-146 27928554-7 2016 Further, Bleo inducetion of both AGT protein and of caspase-9 were prevented by the ACE inhibitor lisinopril. Bleomycin 9-13 caspase 9 Mus musculus 52-61 27928554-7 2016 Further, Bleo inducetion of both AGT protein and of caspase-9 were prevented by the ACE inhibitor lisinopril. Lisinopril 98-108 caspase 9 Mus musculus 52-61 27580936-3 2016 Treatment with caspase-9 inhibitor z-LEHD-FMK in HepG2 cells, AML12 cells and C57BL/b6N mice exacerbated CCl4-induced acute hepatocellular damage, and also down-regulated autophagy markers expression levels, indicating that caspase-9 inhibition may aggravate acute liver damage by suppressing cytoprotective autophagy. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 35-45 caspase 9 Mus musculus 224-233 25647812-4 2016 The results showed that endosulfan significantly improved the expressions of cytochrome c and B-cell lymphoma 2 (Bcl-2)-associated X protein and increased the activities of caspases 9 and 3 as well as the downregulation of the expression of Bcl-2 in GC-1 spg cells. Endosulfan 24-34 caspase 9 Mus musculus 173-189 27310206-5 2016 In relation to increased apoptosis, bax, cleaved caspase-9 and cleaved caspase-3 levels elevated significantly, indicating that PFOS induced germ cell apoptosis by activating the mitochondrial pathway. perfluorooctane sulfonic acid 128-132 caspase 9 Mus musculus 49-58 27286704-0 2016 Exploration of Bcl-2 family and caspases-dependent apoptotic signaling pathway in Zearalenone-treated mouse endometrial stromal cells. Zearalenone 82-93 caspase 9 Mus musculus 32-40 27286704-6 2016 The enzymatic activity assays revealed that caspases-3 and caspase-9 were activated by ZEA treatment in a dose-dependent manner. Zearalenone 87-90 caspase 9 Mus musculus 59-68 27286704-8 2016 Overall, the results suggested that ZEA induced obvious apoptosis in ESCs via a Bcl-2 family and caspases-dependent signaling pathway. Zearalenone 36-39 caspase 9 Mus musculus 97-105 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 27470360-0 2016 Carnosic acid nanoparticles suppress liver ischemia/reperfusion injury by inhibition of ROS, Caspases and NF-kappaB signaling pathway in mice. salvin 0-13 caspase 9 Mus musculus 93-101 27470360-10 2016 And carnosic acid nanoparticles also suppressed the ischemia/reperfusion-induced up-regulation in the pro-apoptotic protein and mRNA levels of Bax, Cyto-c, Apaf-1 and Caspase-9/3 while increased ischemia/reperfusion-induced decrease of anti-apoptotic factor of Bcl-2. salvin 4-17 caspase 9 Mus musculus 167-176 27558076-8 2016 Bupivacaine induced increased expression of caspase-3 and caspase-9, but not caspase-8, indicating that the mitochondrial pathway but not the death receptor apoptosis pathway was activated. Bupivacaine 0-11 caspase 9 Mus musculus 58-67 27558076-9 2016 GM-1 pretreatment inhibited bupivacaine-induced apoptosis and the expression of caspase-3 and caspase-9 in a dose-dependent manner. G(M1) Ganglioside 0-4 caspase 9 Mus musculus 94-103 27605885-8 2016 Treatment with caspase-9 inhibitor ameliorated the decrease in Rubicon protein expression at 10 h of PA and resulted in enlarged AML12 cells under PA treatment. Palmitates 101-103 caspase 9 Mus musculus 15-24 27605885-8 2016 Treatment with caspase-9 inhibitor ameliorated the decrease in Rubicon protein expression at 10 h of PA and resulted in enlarged AML12 cells under PA treatment. Palmitates 147-149 caspase 9 Mus musculus 15-24 27605885-9 2016 The enlargement of AML12 cells by PA with caspase-9 inhibition was canceled by Rubicon knockdown. Palmitates 34-36 caspase 9 Mus musculus 42-51 26066906-7 2016 In addition, NaAsO2 significantly (P<0.05-0.01) altered the expression of intrinsic (Bad , Bcl-2 , cleaved-caspase 3 and cleaved-caspase 9 ) and extrinsic (Fas , Bid , cleaved-caspase 8 ) transcription proteins participating in the apoptotic event. sodium arsenite 13-19 caspase 9 Mus musculus 133-142 27144503-7 2016 A decline in the relative fluorescence emission upon staining S-180 cells with Rhodamine 123 (Rh 123), enhanced expression of cytosolic Cyt c and mitochondrial Bax, and inhibition of apoptosis in the presence of caspase-9 inhibitor in PJE-treated cells indicated intrinsic pathway of apoptosis. Rhodamine 123 79-92 caspase 9 Mus musculus 212-221 27271364-3 2016 Climacostol caused a reduction of viability/proliferation of B16-F10 mouse melanoma cells, a rapidly occurring DNA damage, and induced the intrinsic apoptotic pathway characterised by the dissipation of the mitochondrial membrane potential, the translocation of Bax to the mitochondria, the release of Cytochrome c from the mitochondria, and the activation of Caspase 9-dependent cleavage of Caspase 3. climacostol 0-11 caspase 9 Mus musculus 360-369 27012990-6 2016 In addition, GD blocked the phosphorylation of p38 and inhibited cleaved caspase-9 and DNA damage. decan-4-olide 13-15 caspase 9 Mus musculus 73-82 26804061-3 2016 Our studies indicated that DMAKO-05 not only inhibited B16F0 proliferation and migration but also led to cell cycle arrest at G1 phase and cell apoptosis, in which DMAKO-05 triggered mitochondrial-mediated apoptosis signal including caspase-9/3 and PARP. dmako-05 27-35 caspase 9 Mus musculus 233-242 26804061-3 2016 Our studies indicated that DMAKO-05 not only inhibited B16F0 proliferation and migration but also led to cell cycle arrest at G1 phase and cell apoptosis, in which DMAKO-05 triggered mitochondrial-mediated apoptosis signal including caspase-9/3 and PARP. dmako-05 164-172 caspase 9 Mus musculus 233-242 25409916-8 2016 Furthermore, the transcriptional status and the activities of Caspase 9 and Caspase 3 were increased significantly in the liver when exposed to high doses of Cd, Cr or their mixture. Cadmium 158-160 caspase 9 Mus musculus 62-71 25409916-8 2016 Furthermore, the transcriptional status and the activities of Caspase 9 and Caspase 3 were increased significantly in the liver when exposed to high doses of Cd, Cr or their mixture. Chromium 162-164 caspase 9 Mus musculus 62-71 26968952-7 2016 Furthermore, CoQ0 treatment induced apoptosis through caspase-9/-3 activation, PARP degradation, Bcl-2/Bax dysregulation, and p53 expression. ubiquinone-O 13-17 caspase 9 Mus musculus 54-63 26980746-4 2016 By reducing the metabolic flux through the mevalonate pathway, NZ lowered the activity of Ras/ERK1/2/HIF-1alpha axis and the expression of P-glycoprotein, decreased the glycolysis and the mitochondrial respiratory chain, induced a cytochrome c/caspase 9/caspase 3-dependent apoptosis, thus restoring the direct cytotoxic effects of doxorubicin on tumor cell. Mevalonic Acid 43-53 caspase 9 Mus musculus 244-253 26980746-4 2016 By reducing the metabolic flux through the mevalonate pathway, NZ lowered the activity of Ras/ERK1/2/HIF-1alpha axis and the expression of P-glycoprotein, decreased the glycolysis and the mitochondrial respiratory chain, induced a cytochrome c/caspase 9/caspase 3-dependent apoptosis, thus restoring the direct cytotoxic effects of doxorubicin on tumor cell. Doxorubicin 332-343 caspase 9 Mus musculus 244-253 27149123-9 2016 Flavopiridol enhanced caspase 3/7 and caspase 9 activities in vitro and in vivo in a dose dependent manner via the mitochondrial apoptotic pathway. alvocidib 0-12 caspase 9 Mus musculus 38-47 26329999-9 2016 The expressions of apoptotic proteins caspase 12 and cleaved caspase 9 and caspase 3 were also significantly controlled in ZnS-NPs-treated primary MRPE cells when comparing with thapsigargin- and hydrogen peroxide-treated cells. Zinc 123-126 caspase 9 Mus musculus 61-70 26329999-9 2016 The expressions of apoptotic proteins caspase 12 and cleaved caspase 9 and caspase 3 were also significantly controlled in ZnS-NPs-treated primary MRPE cells when comparing with thapsigargin- and hydrogen peroxide-treated cells. Thapsigargin 178-190 caspase 9 Mus musculus 61-70 26676762-12 2016 Additionally, 661W cells exposed to sodium formate for 24 h exhibited increased levels of p-JNK, Bax, cleaved caspase-3, cleaved caspase-9 and LC3II (the phosphatidylethanolamine-modified form of LC3), although the level of Bcl-2 was decreased. formic acid 36-50 caspase 9 Mus musculus 129-138 27029485-4 2016 Caffeic acid (CA) inhibits JAK-STAT3 signaling, thereby induces apoptotic cell death by upregulating Bax, Cytochrome-C, Caspase-9 and Caspase-3 expression in mouse skin. caffeic acid 0-12 caspase 9 Mus musculus 120-129 26918825-10 2016 Hex also ameliorated STZ-induced expression of cleaved Caspase-9 and the Bax in beta-cells. hexarelin 0-3 caspase 9 Mus musculus 55-64 26918825-10 2016 Hex also ameliorated STZ-induced expression of cleaved Caspase-9 and the Bax in beta-cells. Streptozocin 21-24 caspase 9 Mus musculus 55-64 26581638-0 2016 The carbonic anhydrase inhibitor methazolamide prevents amyloid beta-induced mitochondrial dysfunction and caspase activation protecting neuronal and glial cells in vitro and in the mouse brain. Methazolamide 33-46 caspase 9 Mus musculus 107-114 26581638-5 2016 MTZ prevented DNA fragmentation, CytC release and activation of caspase 9 and caspase 3 induced by Abeta in neuronal and glial cells in culture through the inhibition of mitochondrial hydrogen peroxide production. Methazolamide 0-3 caspase 9 Mus musculus 64-73 26581638-7 2016 Our results, delineating the molecular mechanism of action of MTZ against Abeta-mediated mitochondrial dysfunction and caspase activation, and demonstrating its efficiency in a model of acute amyloid-mediated toxicity, provide the first combined in vitro and in vivo evidence supporting the potential of a new therapy employing FDA-approved CAIs in AD. Methazolamide 62-65 caspase 9 Mus musculus 119-126 26804704-6 2016 Blockade of caspase 9, relative to other caspases, was most protective against both MRZ and BTZ. marizomib 84-87 caspase 9 Mus musculus 12-21 26804704-6 2016 Blockade of caspase 9, relative to other caspases, was most protective against both MRZ and BTZ. marizomib 84-87 caspase 9 Mus musculus 41-49 26804704-6 2016 Blockade of caspase 9, relative to other caspases, was most protective against both MRZ and BTZ. Bortezomib 92-95 caspase 9 Mus musculus 12-21 26804704-6 2016 Blockade of caspase 9, relative to other caspases, was most protective against both MRZ and BTZ. Bortezomib 92-95 caspase 9 Mus musculus 41-49 25577170-10 2016 Furthermore, atorvastatin decreased the levels of cytosolic cytochrome C, Bax, cleaved caspase-9, and cleaved caspase-3, which are associated with death in oxidative stress-injured NSC-34D cells. Atorvastatin 13-25 caspase 9 Mus musculus 87-96 27189473-4 2016 Blockage of sigma -1R significantly inhibited the increased pro-apoptotic proteins such as Bax, Caspase-3 and Caspase-9 induced by methamphetamine. Methamphetamine 131-146 caspase 9 Mus musculus 110-119 27633039-10 2016 A study in mice deficient in PON1 showed that in this experimental model, metformin administration increased the severity of steatosis, increased CCL2 expression, did not activate AMPK, and increased the expression of the apoptosis marker caspase-9. Metformin 74-83 caspase 9 Mus musculus 239-248 27738547-7 2016 Furthermore, Sal could increase the phosphorylation level of Akt and GSK3beta, upregulate the ratio of Bcl-2/Bax, and inhibit the activation of caspase-3, caspase-6, and caspase-9. rhodioloside 13-16 caspase 9 Mus musculus 170-179 26598234-9 2015 Transfection of miR-223 KO hepatocytes with miR-223 mimic enhanced Jo2-induced activation of caspase-3, caspase-8, and caspase-9, whereas transfection of WT hepatocytes with the miR-223 inhibitor attenuated Jo2-induced apoptosis. 2-[[(3~{S})-2,5-bis(oxidanylidene)pyrrolidin-3-yl]carbamoyl]-4-nitro-benzoic acid 67-70 caspase 9 Mus musculus 119-128 26076811-9 2015 Further, quercetin improves apoptotic potential, as observed by the levels of caspase 3, caspase 9, PARP, PKCdelta, and nuclear condensation. Quercetin 9-18 caspase 9 Mus musculus 89-98 26586942-6 2015 EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis. epigallocatechin gallate 0-4 caspase 9 Mus musculus 113-122 26586942-6 2015 EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis. theaflavin 9-11 caspase 9 Mus musculus 113-122 26586942-6 2015 EGCG and TF-NPs were also found to be more effective than bulk TF/EGCG in inducing the cleavage of caspase-3 and caspase-9 and Bax/Bcl2 ratio in favor of apoptosis. epigallocatechin gallate 66-70 caspase 9 Mus musculus 113-122 25968954-6 2015 Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Tunicamycin 10-21 caspase 9 Mus musculus 110-119 26722597-5 2015 Our results showed that treatment with Dex caused cell injury, increased cytosol cytochrome c level and Nox expression, induced apoptosis in caspase-9-dependent manner, and enhanced reactive oxygen species (ROS) production. Dexamethasone 39-42 caspase 9 Mus musculus 141-150 26333892-10 2015 Supplementation of TGF mice with a mixture of red grape polyphenols (50 mg/kg/d) for 4 wk improved mitochondrial function and highly decreased caspases activation, which allowed muscle atrophy mitigation. Polyphenols 56-67 caspase 9 Mus musculus 143-151 26395757-5 2015 Meanwhile, two different zincs inhibited the ZEA-induced loss of mitochondrial membrane potential and elevation of late-stage apoptosis via activating the mitochondrial apoptotic pathway by recovering the mRNA and protein expression of pro-apoptotic genes (Bax, Casp3, Casp9). Zinc 25-30 caspase 9 Mus musculus 269-274 26395757-5 2015 Meanwhile, two different zincs inhibited the ZEA-induced loss of mitochondrial membrane potential and elevation of late-stage apoptosis via activating the mitochondrial apoptotic pathway by recovering the mRNA and protein expression of pro-apoptotic genes (Bax, Casp3, Casp9). Zearalenone 45-48 caspase 9 Mus musculus 269-274 26138643-7 2015 We detected substantial increases in markers of apoptosis including PARP-1, APAF-1, caspase-9, BCL2, and HMGB1, and these increases were attenuated in mice that were nursed by DHA-supplemented dams during the perinatal period. Docosahexaenoic Acids 176-179 caspase 9 Mus musculus 84-93 26031348-9 2015 L-NAT inhibits the secretion of Substance P and IL-1beta, and caspase-1 activation, the release of cytochrome c/Smac/AIF, and the activation of caspase -9, and -3, as well as proteasomal dysfunction. l-nat 0-5 caspase 9 Mus musculus 144-162 26366090-7 2015 Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells. cordycepin 10-20 caspase 9 Mus musculus 99-108 26366090-7 2015 Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells. Cisplatin 26-35 caspase 9 Mus musculus 99-108 26366090-7 2015 Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells. Paclitaxel 43-53 caspase 9 Mus musculus 99-108 25924656-13 2015 (iii) Melamine exposed oocytes had higher rates of abnormal mitochondrial distributions and early stage apoptosis/autophagy, which were shown by increased microtubule-associated protein 1 light chain 3 (LC3) protein expression level and caspase 9, autophagy-related protein 14 (atg14), and lc3 mRNA levels. melamine 6-14 caspase 9 Mus musculus 237-246 26113535-6 2015 We show that Foxc2 reduces the expression of Bax, caspase-9, and caspase-3 in both serum-starved and palmitic acid-induced cell apoptotic models, which confirms the anti-apoptotic role of Foxc2. Palmitic Acid 101-114 caspase 9 Mus musculus 50-59 25858697-8 2015 Furthermore, melatonin decreased Abeta1-42 -induced apoptosis through decreasing the overexpression of caspase-9, caspase-3, and PARP-1 level. Melatonin 13-22 caspase 9 Mus musculus 103-112 26222683-9 2015 Moreover, baicalein preserved mitochondrial respiratory enzyme activities and inhibited cisplatin-induced apoptosis by suppressing p53 expression, Bax/Bcl-2 imbalance, cytochrome c release and activation of caspase-9, caspase-3 and PARP. baicalein 10-19 caspase 9 Mus musculus 207-216 26176694-7 2015 The levels of cleaved caspase-3, cleaved PARP (the substrate of caspase-3) and caspase-9 (the modulator of the caspase-3), which had increased following IR injury, were significantly inhibited by NSP in both wild type and tPA-/- mice. Tetradecanoylphorbol Acetate 222-225 caspase 9 Mus musculus 79-88 25959028-4 2015 In addition to reactive oxygen species scavenging activity in Dex-induced splenocytes, BA administration up-regulated antioxidant enzymes, decreased lipid peroxidation, restored mitochondrial function, decreased the expression of pro-apoptotic protein Bax, prevented the decline of anti-apoptotic protein Bcl-2, inhibited caspase-9 and caspase-3 activation, and improved cell survival. betulinic acid 87-89 caspase 9 Mus musculus 322-331 25839806-5 2015 Furthermore, the protein expression of caspase-9, caspase-3 and cleaved PARP became evident in tumor tissues from mice following TRP treatment, but caspase-8 keep unchanged. Tryptophan 129-132 caspase 9 Mus musculus 39-48 25391371-12 2015 Thiostrepton also induced dose- and time-dependent apoptosis of LSCC cells by down-regulation of Bcl-2, up-regulation of Bax and p53, and inducing release of cytochrome c accompanied by activation of cleaved caspase-9, cleaved caspase-3 and cleaved PARP. Thiostrepton 0-12 caspase 9 Mus musculus 208-217 25824411-4 2015 Our results demonstrated that 4-ACGC possessed notable anti-tumor activity on lung cancer in vivo and in vitro; the mechanisms were involved in inducing mitochondria-mediated apoptosis via up-regulations of caspase-3, caspase-9, Bad and Bax, and down-regulation of Bcl-2. 4-acgc 30-36 caspase 9 Mus musculus 218-227 25915780-7 2015 Exposure of tumor cells to either free SN-38 or IMMU-132 demonstrated the same signaling pathways, with pJNK1/2 and p21(WAF1/Cip1) upregulation followed by cleavage of caspases 9, 7, and 3, ultimately leading to poly-ADP-ribose polymerase cleavage and double-stranded DNA breaks. Irinotecan 39-44 caspase 9 Mus musculus 168-188 25359171-3 2015 Further, BP treatment brought about a significant decrease in the activities of caspase 3, caspase 9 as well as the number of apoptotic cells. Benzo(a)pyrene 9-11 caspase 9 Mus musculus 91-100 25913086-7 2015 The production of excessive ROS was NADPH oxidase-dependent, which contributed to mitochondrial structural damage and mitochondrial dysfunction in placentas, followed by the cleavage of caspase-9 and caspase-3, and finally resulted in apoptosis of trophoblasts. Reactive Oxygen Species 28-31 caspase 9 Mus musculus 186-195 25736991-6 2015 Our experimental evidence suggests that ATO exposure induces apoptotic cell deathby the activation of caspase-3 and reciprocal regulation of Bcl-2/Bax with the concomitant reduction of mitochondrial membrane potential and increased level of cytosolic cytochrome c, Apaf1, caspase-9. Atorvastatin 40-43 caspase 9 Mus musculus 272-281 25639715-5 2015 H9 and co-treatment with PEM induced the cleavage of proapoptotic factors, such as caspase-3, caspase-8, caspase-9, and poly(ADP)-ribose polymerase (PARP). Pemetrexed 25-28 caspase 9 Mus musculus 105-114 25680694-13 2015 Finally, we found that exposure to Nano-ZnO caused increased ER stress-associated apoptotic protein levels, such as caspase-3, caspase-9, caspase-12, phosphorylation of JNK, and CHOP/GADD153, and up-regulation of pro-apoptotic genes (chop and bax). Zinc Oxide 40-43 caspase 9 Mus musculus 127-136 25619426-7 2015 The cytotoxic effect of phytanic acid was also abolished by a caspase-9 inhibitor. Phytanic Acid 24-37 caspase 9 Mus musculus 62-71 25359171-5 2015 Also, supplementation with curcumin and quercetin separately to BP-treated mice brought a significant improvement in the enzyme activities of caspase 9 as well as caspase 3 but the improvement was more pronounced following combined treatment. Curcumin 27-35 caspase 9 Mus musculus 142-151 25359171-5 2015 Also, supplementation with curcumin and quercetin separately to BP-treated mice brought a significant improvement in the enzyme activities of caspase 9 as well as caspase 3 but the improvement was more pronounced following combined treatment. Quercetin 40-49 caspase 9 Mus musculus 142-151 25359171-5 2015 Also, supplementation with curcumin and quercetin separately to BP-treated mice brought a significant improvement in the enzyme activities of caspase 9 as well as caspase 3 but the improvement was more pronounced following combined treatment. Benzo(a)pyrene 64-66 caspase 9 Mus musculus 142-151 25478867-3 2015 DMBA treatment suppressed Bax, Bax/Bcl-2 ratio, release of cyt c, Apaf1, caspase-9, -3 mediated apoptosis. 9,10-Dimethyl-1,2-benzanthracene 0-4 caspase 9 Mus musculus 73-82 25478867-5 2015 Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3. Butyric Acid 28-30 caspase 9 Mus musculus 210-219 25478867-5 2015 Simultaneous application of BA, NA and CAG induced a mitochondria-mediated apoptosis, characterized by a rise in the Bax, Bax/Bcl-2 ratio, release of cyt c, upregulation of Apaf1 with down-stream activation of caspase-9, -3. Glucaric Acid 39-42 caspase 9 Mus musculus 210-219 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Thioctic Acid 13-16 caspase 9 Mus musculus 163-172 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Trinitrobenzenesulfonic Acid 41-45 caspase 9 Mus musculus 163-172 26406155-4 2015 Results demonstrated that Sirt 1 and Bcl-2 were inhibited, whereas p53 acetylation, Bax, and caspase 9 were promoted by H2O2, as was aggravated by the Sirt 1 inhibitor, EX-527. Hydrogen Peroxide 120-124 caspase 9 Mus musculus 93-102 26406155-5 2015 Instead, RSV inhibited the H2O2-induced both p53 acetylation and the caspase 9 activation, whereas ameliorated the H2O2-induced Bcl-2 inhibition and apoptosis. Resveratrol 9-12 caspase 9 Mus musculus 69-78 26406155-5 2015 Instead, RSV inhibited the H2O2-induced both p53 acetylation and the caspase 9 activation, whereas ameliorated the H2O2-induced Bcl-2 inhibition and apoptosis. Hydrogen Peroxide 27-31 caspase 9 Mus musculus 69-78 25349173-7 2014 We found that the burden of DNA damage was increased in Casp9-deficient cells after exposure to the alkylator, N-ethyl-nitrosourea (ENU). Ethylnitrosourea 111-130 caspase 9 Mus musculus 56-61 25401971-11 2015 Moreover, melatonin lowered the oxidative stress kinase p-JNK which suppressed various apoptotic markers, that is, cytochrome C, caspase-9, caspase-3 and PARP-1, and prevent neurodegeneration. Melatonin 10-19 caspase 9 Mus musculus 129-138 24848512-0 2015 Glycoursodeoxycholic acid reduces matrix metalloproteinase-9 and caspase-9 activation in a cellular model of superoxide dismutase-1 neurodegeneration. glycoursodeoxycholic acid 0-25 caspase 9 Mus musculus 65-74 24848512-10 2015 GUDCA exerted preventive effects (p < 0.05) while also reduced caspase-9 levels when added at 2 DIV (p < 0.05). glycoursodeoxycholic acid 0-5 caspase 9 Mus musculus 63-72 24748476-7 2014 The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1. Doxorubicin 90-93 caspase 9 Mus musculus 267-276 25406029-7 2014 In addition, we observed that AAI markedly increases the expression of pro-apoptotic proteins, including Bax, caspase-3, caspase-9, and poly(ADP) ribose polymerase (PARP). aristolochic acid I 30-33 caspase 9 Mus musculus 121-130 24748476-7 2014 The study in primary embryonic cell lines showed that the apoptosis after incubation with DOX was reduced in cells overexpressing Hsp70 (Tg/Tg), while the apoptotic pathway that was activated by DOX administration involved activated protein factors such as p53, Bax, caspase-9, caspase-3, and PARP-1. Doxorubicin 195-198 caspase 9 Mus musculus 267-276 25046589-9 2014 LPS/d-GalN induced apoptosis of hepatocytes, as estimated by caspase 3, caspase 8 and caspase 9 activations. Deuterium 4-5 caspase 9 Mus musculus 86-95 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Leucine 14-21 caspase 9 Mus musculus 153-162 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Tyrosine 23-31 caspase 9 Mus musculus 153-162 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Arginine 33-41 caspase 9 Mus musculus 153-162 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Homoarginine 43-55 caspase 9 Mus musculus 153-162 25333616-5 2014 We found that leucine, tyrosine, arginine, homoarginine or glucose treatment of the GA1 model cells reduced the gene expression of caspase-3, caspase-8, caspase-9, bax, fos, and jun and restored the intracellular NADH and ATP levels. Glucose 59-66 caspase 9 Mus musculus 153-162 25290208-8 2014 Perindopril significantly decreased caspase-3 and caspase-9 activities, and elevated Bcl-2/Bax ratio in the hippocampus. Perindopril 0-11 caspase 9 Mus musculus 50-59 25109418-7 2014 Furthermore, celecoxib induced apoptosis via the loss of the mitochondrial transmembrane potential (DeltaPsim), the release of cytochrome c and AIF, and the activation of caspase-9 and caspase-3. Celecoxib 13-22 caspase 9 Mus musculus 171-180 25090966-6 2014 Furthermore, the overexpression of Sirt3 attenuated the release of cytochrome c, the increase in the Bax/Bcl-2 ratio, as well as caspase-9/caspase-3 activity induced by H(2)O(2), and eventually inhibited apoptotic neuronal cell death. Hydrogen Peroxide 169-177 caspase 9 Mus musculus 129-138 24998494-7 2014 Diazoxide (250-500x10(-6)M), a SUR1-2B/Kir6.2 channel opener, prevented the protein loss induced by STS in the slow-twitch muscle after 6h showing an EC50 of 1.35x10(-7)M and Emax of 75%, down-regulated the caspase-9 gene and enhanced the KATP currents. Diazoxide 0-9 caspase 9 Mus musculus 207-216 25278835-5 2014 Quantitative real-time PCR (qPCR) data revealed that the expression of apoptotic markers, including Casp3 and Casp9, was significantly higher when neomycin was injected from P8 to P14, while the expression of the X-linked inhibitor of apoptosis protein (XIAP) gene was significantly higher when neomycin was injected from P60 to P66. Neomycin 147-155 caspase 9 Mus musculus 110-115 25222049-10 2014 Moreover, Bazhen decoction down-regulate acetaminophen-induced Bax/Bcl-2 ratio, caspase 3, caspase 8 and caspase 9. Acetaminophen 41-54 caspase 9 Mus musculus 105-114 25028793-9 2014 Moreover, adiponectin treatment prevented palmitate-induced apoptosis by inhibition of caspase-9 activation, but not of caspase-8, and induced an upregulation of BCL-2 and a downregulation of Bax in protein level. Palmitates 42-51 caspase 9 Mus musculus 87-96 24661197-3 2014 Here, we show that silica and double-stranded RNA (dsRNA) synergistically induces caspase-9-dependent apoptosis, but not inflammasome activation, of bronchial epithelial cells. Silicon Dioxide 19-25 caspase 9 Mus musculus 82-91 25074826-6 2014 We found that fluoride exposure affected the expression levels of stress response factors, signal transduction components, and apoptosis-related proteins, including caspase-3/caspase-9, B-cell lymphoma 2 (Bcl-2), and Bax. Fluorides 14-22 caspase 9 Mus musculus 175-184 25016646-8 2014 Western blotting study revealed that the induction apoptosis of S-65 cancer cells by curcumin micelles was mainly due to the down-regulation of p-Rb, Blc-2, p-AKT expression and caspase-9 activation. Curcumin 85-93 caspase 9 Mus musculus 178-187 24739012-9 2014 Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment. Lenalidomide 142-154 caspase 9 Mus musculus 82-91 24859647-3 2014 This study demonstrated that DDT-induced apoptosis of mouse embryonic neuronal cells is a caspase-9-, caspase-3-, and GSK-3beta-dependent process, which involves p,p"-DDT-specific impairment of classical ERs. DDT 29-32 caspase 9 Mus musculus 90-99 24859647-3 2014 This study demonstrated that DDT-induced apoptosis of mouse embryonic neuronal cells is a caspase-9-, caspase-3-, and GSK-3beta-dependent process, which involves p,p"-DDT-specific impairment of classical ERs. DDT 162-170 caspase 9 Mus musculus 90-99 24768735-6 2014 In addition, GE attenuated the expression of apoptotic markers evident by the normalized Bcl-2/Bax ratio and decreased expression of cytochrome-C and caspase-9 in the substantia nigra and striatum of MPTP/p induced mice model of PD. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 200-204 caspase 9 Mus musculus 150-159 24952344-3 2014 MTEC1 cell apoptosis induced by DON was confirmed by nuclei morphology change, TUNEL positive staining, annexin V/propidium iodide positive staining and increased protein levels of caspase-3, caspase-8, caspase-9 and poly(ADP-ribose) polymerase (PARP). deoxynivalenol 32-35 caspase 9 Mus musculus 203-212 24830863-5 2014 In the rotenone-pretreated group, the elevation of hepatic caspase-3, caspase-8 and caspase-9 activities induced by LPS/D-Gal decreased and rotenone reduced the count of TUNEL-positive apoptotic hepatocytes. Rotenone 7-15 caspase 9 Mus musculus 84-93 24964211-6 2014 Cerulenin and orlistat treatments were found to induce apoptosis and decrease cell proliferation, in addition to inducing the release of mitochondrial cytochrome c and activating caspases-9 and -3. Cerulenin 0-9 caspase 9 Mus musculus 179-196 24964211-6 2014 Cerulenin and orlistat treatments were found to induce apoptosis and decrease cell proliferation, in addition to inducing the release of mitochondrial cytochrome c and activating caspases-9 and -3. Orlistat 14-22 caspase 9 Mus musculus 179-196 24922073-8 2014 In addition, we show that the cell death induced by 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP), a toxin that activates Casp9-dependent apoptosis in mDA neurons, is attenuated in adult mBACtgDyrk1a mice, leading to an increased survival of SN DA neurons 21 days after MPTP intoxication. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 52-96 caspase 9 Mus musculus 128-133 24922073-8 2014 In addition, we show that the cell death induced by 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP), a toxin that activates Casp9-dependent apoptosis in mDA neurons, is attenuated in adult mBACtgDyrk1a mice, leading to an increased survival of SN DA neurons 21 days after MPTP intoxication. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 98-102 caspase 9 Mus musculus 128-133 24922073-8 2014 In addition, we show that the cell death induced by 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP), a toxin that activates Casp9-dependent apoptosis in mDA neurons, is attenuated in adult mBACtgDyrk1a mice, leading to an increased survival of SN DA neurons 21 days after MPTP intoxication. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 276-280 caspase 9 Mus musculus 128-133 24752940-0 2014 Effect of cortisol on caspases in the co-cultured C2C12 and 3 T3-L1 cells. Hydrocortisone 10-18 caspase 9 Mus musculus 22-30 24781573-13 2014 remifentanil inhibited cortical Bax protein expression, caspase-9 activity, and preserved mitochondrial integrity, whereas it had no effect on caspase-8 activity. Remifentanil 0-12 caspase 9 Mus musculus 56-65 24811863-8 2014 We have also shown that the Met-F-AEA in combination with URB597 induces G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4 expressions, ultimately leading to apoptosis via activation of caspase-9 and PARP. 2-methylarachidonyl-2'-fluoroethylamide 28-37 caspase 9 Mus musculus 197-206 24811863-8 2014 We have also shown that the Met-F-AEA in combination with URB597 induces G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4 expressions, ultimately leading to apoptosis via activation of caspase-9 and PARP. cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester 58-64 caspase 9 Mus musculus 197-206 24739733-8 2014 Conversely, we found that treatment of specific JNK inhibitor SP600125 suppressed the cleavages of caspase 9/3 and PARP induced by hUCMSCs in PC-3 cells by Western blotting and immunofluorescence assay. pyrazolanthrone 62-70 caspase 9 Mus musculus 99-108 25898737-4 2014 At the same cell death level, activity of caspase-3 and caspase-9 in the cells incubated with 14G2a was about 7.5- and 3-fold lower than in cells after incubation with staurosporine. Staurosporine 168-181 caspase 9 Mus musculus 56-65 25898737-6 2014 At the same conditions, pan caspase inhibitor decreased staurosporine-induced apoptosis at 55-65%. Staurosporine 56-69 caspase 9 Mus musculus 28-35 24705375-6 2014 On the other hand, enzyme activities of caspase 3 and caspase 9 were noticed to be significantly decreased following BP treatment. Benzo(a)pyrene 117-119 caspase 9 Mus musculus 54-63 24705375-10 2014 However, the enzyme activities of caspase 3 and caspase 9 showed a significant increase upon treatment with curcumin and resveratrol. Curcumin 108-116 caspase 9 Mus musculus 48-57 24705375-10 2014 However, the enzyme activities of caspase 3 and caspase 9 showed a significant increase upon treatment with curcumin and resveratrol. Resveratrol 121-132 caspase 9 Mus musculus 48-57 24849190-4 2014 Western blot analysis was also used to measure the expression level of Bcl-2, Bax, caspase 9, and caspase 3 proteins in H2O2-treated RGC-5 cells. Hydrogen Peroxide 120-124 caspase 9 Mus musculus 83-92 24682087-8 2014 Furthermore, prazosin and yohimbine protected against restraint-induced hepatocytes apoptosis through attenuating the activation of caspases-9 and -3 and reducing the Bax/Bcl-2 ratio. Prazosin 13-21 caspase 9 Mus musculus 132-149 24682087-8 2014 Furthermore, prazosin and yohimbine protected against restraint-induced hepatocytes apoptosis through attenuating the activation of caspases-9 and -3 and reducing the Bax/Bcl-2 ratio. Yohimbine 26-35 caspase 9 Mus musculus 132-149 24508257-2 2014 The processing is best characterized for the mouse enzyme, where di-asparate DD motifs mediate the production of active ~55 and ~60 kDa isoforms from the ~74 kDa precursor in a caspase-9 dependent manner. di-asparate 65-76 caspase 9 Mus musculus 177-186 24568162-4 2014 We observed inhibition of NF-kappaB nuclear translocation, up-regulation of Bax and down-regulation of Bcl-2, as well as increased caspase-3 and caspase-9 expression after baicalin treatment in vitro and in vivo, which indicates that the mitochondrial pathway was involved in baicalin-induced apoptosis. baicalin 172-180 caspase 9 Mus musculus 145-154 25503322-8 2014 Exposure to YLT26 induced mitochondrial transmembrane potential ( Psim) change, activated caspase-9, and downregulated the Bcl-2 expression, as well as enhanced ROS accumulation in 4T1 cells. ylt26 12-17 caspase 9 Mus musculus 90-99 24643139-9 2014 Here we showed that the propofol treatment improved cognitive function and attenuated brain caspase-3 and caspase-9 activation in both aged WT and AD Tg mice. Propofol 24-32 caspase 9 Mus musculus 106-115 24849190-6 2014 MDHB also obstructed H2O2-induced apoptosis by regulating the expression of Bcl-2 and Bax, as well as suppressing the activation of caspase 9 and caspase 3. methyl 3,4-dihydroxybenzoate 0-4 caspase 9 Mus musculus 132-141 25376384-10 2014 Macrophage depletion prevented Gly-induced apoptotic death of tubular epithelial cells by decreasing caspase-9, ERK and p53, while increasing Bcl-2 expression. Glycerol 31-34 caspase 9 Mus musculus 101-110 24868317-9 2014 Curcumin significantly reduced the number of apoptotic cells and inhibited the upregulation of cyt-c, caspase-9, and caspase-3 at 7 days p.i. Curcumin 0-8 caspase 9 Mus musculus 102-111 24436715-15 2013 Here, we demonstrate that soluble factors secreted by the NCD IVD NP strongly protect murine NP cells not only from IL-1beta + FasL but also from Etoposide-induced apoptosis via suppression of activated caspase-9 and caspase-3/7. Etoposide 146-155 caspase 9 Mus musculus 203-212 24200352-4 2013 Moreover, 1 greatly suppressed the secretion of TNF-alpha, IL-6, and IL-1beta, inhibited the degradation of IkappaB alpha, and down-regulated expression of cleaved caspase-3 and cleaved caspase-9 in colon tissues of DSS-treated mice. Dextran Sulfate 216-219 caspase 9 Mus musculus 186-195 23933437-8 2013 In addition, the NQs induced a decrease in the mitochondrial membrane potential and increased the proteolytic activation of caspases 9 and 3 and the cleavage of Poly (ADP-Ribose) Polymerase (PARP). NQS 17-20 caspase 9 Mus musculus 124-140 23685326-6 2013 OKA administration resulted in memory impairment with a decreased cerebral blood flow (CBF) (measured by laser doppler flowmetry), ATP level and increased mitochondrial (Ca(2+))i, neuroinflammation (increased TNF-alpha, IL-1beta, COX-2 and GFAP), oxidative-nitrosative stress, increased Caspase-9 and cholinergic dysfunction (decreased AChE activity/expression and alpha7 nicotinic acetylcholine receptor expression) in cerebral cortex and hippocampus of mice brain. Okadaic Acid 0-3 caspase 9 Mus musculus 287-296 23420823-7 2013 Significant increases in caspase 9 and caspase 3 concentrations were also found in cells treated with >=50 mug/mL CPFX for 24 and 36 hours, respectively (P < .001). Ciprofloxacin 117-121 caspase 9 Mus musculus 25-34 23966082-15 2013 Triterpenes induced apoptosis by decreasing the expression of the antiapoptotic protein Bcl-2 and pro-caspase 9 and increasing the levels of cleaved-caspase 9. Triterpenes 0-11 caspase 9 Mus musculus 102-111 23966082-15 2013 Triterpenes induced apoptosis by decreasing the expression of the antiapoptotic protein Bcl-2 and pro-caspase 9 and increasing the levels of cleaved-caspase 9. Triterpenes 0-11 caspase 9 Mus musculus 149-158 21786383-6 2013 Western blot analysis demonstrated that propofol promoted Fas, cytochrome c, caspase-9 and -3 active form and Bax levels, but inhibited Bcl-xl protein level which led to cell apoptosis. Propofol 40-48 caspase 9 Mus musculus 77-93 23684363-17 2013 Consequently, SNP-enhanced cascade activation of caspases-9 and -3 was decreased by propofol (P < .01). Propofol 84-92 caspase 9 Mus musculus 49-66 33209651-12 2013 Down regulated expression of caspase-9 and caspase-3 proposes a non-canonical pathway of cell death during "ER stress" induced by nano-formulated Tunicamycin. Tunicamycin 146-157 caspase 9 Mus musculus 29-38 23707211-7 2013 Cantharidin treatment caused up-regulation of caspases 9 and -3/7 and a decrease in LDH activity in EAC cells. Cantharidin 0-11 caspase 9 Mus musculus 46-63 23678002-3 2013 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. Cisplatin 41-45 caspase 9 Mus musculus 98-107 23678002-3 2013 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. Aspartic Acid 139-142 caspase 9 Mus musculus 98-107 23678002-3 2013 Here, we demonstrate that treatment with CDDP resulted in down-regulation of c-Jun expression via caspase-9-dependent cleavage of c-Jun at Asp-65 and MEKK1-mediated ubiquitylation and degradation of c-Jun in CDDP-sensitive cancer cells. Cisplatin 208-212 caspase 9 Mus musculus 98-107 23584725-8 2013 Delphinidin attenuated the hypoxia-induced increase in Bax, cleaved caspase-9, cleaved caspase-3, and decrease in Bcl-2, which were diminished by pretreatment of Akt inhibitor. delphinidin 0-11 caspase 9 Mus musculus 68-77 23755271-5 2013 ZnO specifically triggered the intrinsic apoptotic pathway, because Jurkat T lymphocytes deficient in the key mediator caspase-9 were protected against ZnO-mediated toxicity whereas reconstituted cells were not. Zinc Oxide 0-3 caspase 9 Mus musculus 119-128 23824039-11 2013 MPTQ-mediated apoptosis is also associated with increased activation of caspase-9, -3 and -7 but not caspase-2 and -8. 8-methoxypyrimido(4',5'-4,5)thieno(2,3-b)quinoline-4(3H)-one 0-4 caspase 9 Mus musculus 72-92 23755271-5 2013 ZnO specifically triggered the intrinsic apoptotic pathway, because Jurkat T lymphocytes deficient in the key mediator caspase-9 were protected against ZnO-mediated toxicity whereas reconstituted cells were not. Zinc Oxide 152-155 caspase 9 Mus musculus 119-128 23392803-11 2013 LPS/D-GalN-induced caspase-3 and caspase-9 activation was remarkably suppressed by CA-074me. Deuterium 4-5 caspase 9 Mus musculus 33-42 23430060-0 2013 Induction of apoptosis through caspase-independent or caspase-9-dependent pathway in mouse and human osteosarcoma cells by a new nitroxyl spin-labeled derivative of podophyllotoxin. nitroxyl 129-137 caspase 9 Mus musculus 54-63 23430060-0 2013 Induction of apoptosis through caspase-independent or caspase-9-dependent pathway in mouse and human osteosarcoma cells by a new nitroxyl spin-labeled derivative of podophyllotoxin. Podophyllotoxin 165-180 caspase 9 Mus musculus 54-63 23862406-8 2013 These results indicate that bcl-2, caspase-9 and caspase-12 may play significant roles in ZnO nanoparticle-induced RGC-5 cell damage. Zinc Oxide 90-93 caspase 9 Mus musculus 35-44 23525555-8 2013 The levels of caspase-3 mRNA, caspase-3 and cleaved-caspase-3 proteins in the anisomycin-treated EAC cells were augmented in a dose- and time-dependent manner, following the activation of caspase-8 and caspase-9, which finally triggered PARP cleavage. Anisomycin 78-88 caspase 9 Mus musculus 202-211 23525555-8 2013 The levels of caspase-3 mRNA, caspase-3 and cleaved-caspase-3 proteins in the anisomycin-treated EAC cells were augmented in a dose- and time-dependent manner, following the activation of caspase-8 and caspase-9, which finally triggered PARP cleavage. ethyl acetoacetate 97-100 caspase 9 Mus musculus 202-211 23395740-4 2013 The mRNA levels of Caspase3, Caspase8, and Caspase9 increased with the occurrence of early stage apoptosis in oocytes following 5-AzaC treatment. Azacitidine 128-134 caspase 9 Mus musculus 43-51 23637769-13 2013 CONCLUSION: Using the cell-penetrating peptides blocking caspase-9/PP2A interactions, we have demonstrated that DPT-C9h had a strong therapeutic effect in vitro and in vivo in mouse models of tumour progression. dpt-c9h 112-119 caspase 9 Mus musculus 57-66 23280144-9 2013 Guggulsterone induced apoptosis through activation of caspase-8, caspase-9, and caspase-3 in tumor cells. pregna-4,17-diene-3,16-dione 0-13 caspase 9 Mus musculus 65-74 23274307-7 2013 Expression levels of cleaved poly ADP-ribose polymerase (PARP), caspase-9 and caspase-3, markers of apoptosis, were significantly higher in CSO-SA treated cells. cso-sa 140-146 caspase 9 Mus musculus 64-73 23036022-10 2013 Western blot analysis revealed that VPA notably down-regulated the expression of Caspase-3, Caspase-9 and Caspase-12, reduced the level of cytochrome C and Bax. Valproic Acid 36-39 caspase 9 Mus musculus 92-101 23392803-11 2013 LPS/D-GalN-induced caspase-3 and caspase-9 activation was remarkably suppressed by CA-074me. CA 074 methyl ester 83-91 caspase 9 Mus musculus 33-42 22964516-6 2013 Further studies revealed increased caspase-9 and caspase-3/7 activation in VSMC beginning as early as 0.5 and 1h following treatment, respectively. Hydrogen 110-112 caspase 9 Mus musculus 35-44 23228706-4 2013 Fucoxanthin-induced apoptosis was accompanied with the down-regulation of the protein levels of Bcl-xL, an inhibitor of apoptosis proteins (IAPs), resulting in a sequential activation of caspase-9, caspase-3, and PARP. fucoxanthin 0-11 caspase 9 Mus musculus 187-196 23479770-8 2013 Wortmannin intervention improved betacR/EPOR expression, promoted caspase-9 and -3 activation, and increased active caspase-3 positive cells, while renal function and structure, and apoptotic cell counts scarcely changed. Wortmannin 0-10 caspase 9 Mus musculus 66-82 23610522-10 2013 In addition, the PTX-NPs markedly inhibited interleukin-6 secretion, increased caspase-8, caspase-9, and caspase-3 expression, and induced apoptosis of tumor cells in the treated mice. ptx 17-20 caspase 9 Mus musculus 90-99 23182907-8 2013 A lanata treatment resulted in downregulation of bcl-2 and cyclin-D1 expression and upregulation of p53, bax, caspase-9, caspase-3, p21, and p27 gene expression in B16F-10 cells. lanata 2-8 caspase 9 Mus musculus 110-119 23820203-0 2013 Gossypol acetic acid induces apoptosis in RAW264.7 cells via a caspase-dependent mitochondrial signaling pathway. gossypol acetic acid 0-20 caspase 9 Mus musculus 63-70 23820203-4 2013 Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK, respectively. gossypol acetic acid 13-15 caspase 9 Mus musculus 89-96 23820203-4 2013 Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK, respectively. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 108-117 caspase 9 Mus musculus 89-96 23820203-6 2013 Moreover, the ROS production in cells was elevated, and the levels of activated caspase-3 and caspase-9 were up-regulated in a dose-dependent manner. Reactive Oxygen Species 14-17 caspase 9 Mus musculus 94-103 23820203-7 2013 Notably, GA-induced cell apoptosis was markedly inhibited by caspase inhibitors. gossypol acetic acid 9-11 caspase 9 Mus musculus 61-68 23820203-8 2013 These results suggest that GA-induced RAW264.7 cell apoptosis may be mediated via a caspase-dependent mitochondrial signaling pathway. gossypol acetic acid 27-29 caspase 9 Mus musculus 84-91 22434380-5 2012 Western blot data showed that in zinc+H(2)O(2)-treated cells, zinc decreased the levels of AIF, Bax and active caspase-9 and -3, which are pro-apoptotic factors. Hydrogen Peroxide 38-46 caspase 9 Mus musculus 111-127 23027807-9 2012 EtBr treatment also decreased apoptosis and caspase-9 protein expression in old MCs. Ethidium 0-4 caspase 9 Mus musculus 44-53 22847295-4 2012 Annexin V staining and flow cytometry showed that GA-DM treatment induced apoptosis of melanoma cells, which was supported by a detection of increased Bax proteins, co-localization and elevation of Apaf-1 and cytochrome c, and a subsequent cleavage of caspases 9 and 3. 3,7-dioxolanosta-8,24-dien-26-oic acid 50-55 caspase 9 Mus musculus 252-268 22687607-8 2012 Additional bleomycin-induced inflammatory responses reduced by TAPI-0 treatment included inflammatory cell recruitment into the lungs, levels of total protein and lactate dehydrogenase activity in bronchoalveolar lavage fluid, as well as caspase-3 and caspase-9 activity and alveolar epithelial cell apoptosis in lung tissue. Bleomycin 11-20 caspase 9 Mus musculus 252-261 22837216-5 2012 The alantolactone-induced apoptosis was found to be associated with glutathione (GSH) depletion, reactive oxygen species (ROS) generation, mitochondrial transmembrane potential dissipation, cardiolipin oxidation, upregulation of p53 and Bax, downregulation of Bcl-2, cytochrome c release, activation of caspases (caspase 9 and 3), and cleavage of poly (ADP-ribose) polymerase. alantolactone 4-17 caspase 9 Mus musculus 303-311 22837216-5 2012 The alantolactone-induced apoptosis was found to be associated with glutathione (GSH) depletion, reactive oxygen species (ROS) generation, mitochondrial transmembrane potential dissipation, cardiolipin oxidation, upregulation of p53 and Bax, downregulation of Bcl-2, cytochrome c release, activation of caspases (caspase 9 and 3), and cleavage of poly (ADP-ribose) polymerase. alantolactone 4-17 caspase 9 Mus musculus 313-328 22212591-10 2012 Moreover, level of cytosolic cytochrome c and Apaf-1, and activation of caspase-9 and caspase-3 were suppressed in response to cystamine treatment. Cystamine 127-136 caspase 9 Mus musculus 72-81 22137261-6 2012 Furthermore, resveratrol activated the mitochondrial signaling with decreases in the mitochondrial membrane potential, cytochrome c release and the activation of caspase 9 and caspase 3. Resveratrol 13-24 caspase 9 Mus musculus 162-171 22687607-8 2012 Additional bleomycin-induced inflammatory responses reduced by TAPI-0 treatment included inflammatory cell recruitment into the lungs, levels of total protein and lactate dehydrogenase activity in bronchoalveolar lavage fluid, as well as caspase-3 and caspase-9 activity and alveolar epithelial cell apoptosis in lung tissue. TAPI-0 63-69 caspase 9 Mus musculus 252-261 22613767-0 2012 zVAD-fmk upregulates caspase-9 cleavage and activity in etoposide-induced cell death of mouse embryonic fibroblasts. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 0-8 caspase 9 Mus musculus 21-30 22613767-0 2012 zVAD-fmk upregulates caspase-9 cleavage and activity in etoposide-induced cell death of mouse embryonic fibroblasts. Etoposide 56-65 caspase 9 Mus musculus 21-30 22613767-10 2012 In MEFs, zVAD-fmk increased p53-dependent loss of DeltaPsim, cytochrome c release and caspase-9 activity. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 9-17 caspase 9 Mus musculus 86-95 22613767-11 2012 Indeed, zVAD-fmk inhibited effector caspases (caspases-3, -6, -7) as expected but increased caspase-9 cleavage and activity in etoposide-treated MEFs. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 8-16 caspase 9 Mus musculus 92-101 22613767-11 2012 Indeed, zVAD-fmk inhibited effector caspases (caspases-3, -6, -7) as expected but increased caspase-9 cleavage and activity in etoposide-treated MEFs. Etoposide 127-136 caspase 9 Mus musculus 92-101 22613767-12 2012 Q-VD-OPh, another caspase inhibitor, also increased both loss of DeltaPsim and caspase-9 cleavage in etoposide-treated MEFs. Etoposide 101-110 caspase 9 Mus musculus 79-88 22613767-14 2012 Invalidation of caspase-9 did not inhibit mitochondrial membrane depolarization but suppressed zVAD-fmk amplification of this process. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 95-103 caspase 9 Mus musculus 16-25 22613767-15 2012 Altogether, our data suggest that caspase-9 activity is up-regulated by zVAD-fmk and is involved in an amplification loop of etoposide-induced cell death at the mitochondrial level in MEFs. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 72-80 caspase 9 Mus musculus 34-43 22613767-15 2012 Altogether, our data suggest that caspase-9 activity is up-regulated by zVAD-fmk and is involved in an amplification loop of etoposide-induced cell death at the mitochondrial level in MEFs. Etoposide 125-134 caspase 9 Mus musculus 34-43 22281782-3 2012 DPHC slightly reduced the expression of Bax induced by H(2)O(2) but recovered the expression of Bcl-xL as well as caspase-9 and -3 mediated PARP cleavage by H(2)O(2). diphlorethohydroxycarmalol 0-4 caspase 9 Mus musculus 114-130 22293507-9 2012 The levels of two fragments of caspase 9 in the cortex were higher in the control group compared with the hyperbaric oxygen-exposed group 1h after seizures (p<0.01). Oxygen 117-123 caspase 9 Mus musculus 31-40 22293507-9 2012 The levels of two fragments of caspase 9 in the cortex were higher in the control group compared with the hyperbaric oxygen-exposed group 1h after seizures (p<0.01). Hydrogen 138-140 caspase 9 Mus musculus 31-40 22242562-8 2012 Caspase-3, caspase-8 and caspase-9 activities were significantly induced by BisGMA in a dose-dependent manner (P < 0.05). Bisphenol A-Glycidyl Methacrylate 76-82 caspase 9 Mus musculus 25-34 22294729-8 2012 In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737-induced thrombocytopenia in vivo. BH 3 58-61 caspase 9 Mus musculus 22-31 22294729-8 2012 In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737-induced thrombocytopenia in vivo. ABT-737 70-77 caspase 9 Mus musculus 22-31 22294729-8 2012 In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737-induced thrombocytopenia in vivo. Phosphatidylserines 88-106 caspase 9 Mus musculus 22-31 22294729-8 2012 In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737-induced thrombocytopenia in vivo. Phosphatidylserines 108-110 caspase 9 Mus musculus 22-31 22294729-8 2012 In platelets, loss of caspase-9 confers resistance to the BH3 mimetic ABT-737, blocking phosphatidylserine (PS) exposure and delaying ABT-737-induced thrombocytopenia in vivo. ABT-737 134-141 caspase 9 Mus musculus 22-31 22439433-7 2012 Also, oral administration of rosmarinic acid brought back the status of phase I and phase II detoxication agents, lipid peroxidation byproducts, antioxidants and apoptotic markers (p53, Bcl-2, caspase-3 and caspase-9) in DMBA treated mice. rosmarinic acid 29-44 caspase 9 Mus musculus 207-216 21665879-8 2012 Nomilin treatment also exhibited a downregulated Bcl-2 and cyclin-D1 expression and upregulated p53, Bax, caspase-9, caspase-3, p21, and p27 gene expression in B16F-10 cells. nomilin 0-7 caspase 9 Mus musculus 106-115 22259050-11 2012 Consequently, honokiol induced cascade activation of caspases-9, -3, and -6. honokiol 14-22 caspase 9 Mus musculus 53-75 21682651-6 2012 The proapoptotic genes p53, Bax, caspase-9, and caspase-3 were found upregulated in andrographolide-treated cells, whereas the antiapoptotic gene bcl-2 was downregulated. andrographolide 84-99 caspase 9 Mus musculus 33-42 22312258-6 2012 The effects of PTX on the sensitization of L1210/VCR cells to VCR correlate with the stimulation of apoptosis detected by Annexin V/propidium iodide apoptosis necrosis kit and proteolytic activation of both caspase-3 and caspase-9 monitored by Western blot analysis. Pentoxifylline 15-18 caspase 9 Mus musculus 221-230 22687777-7 2012 Quantitative real-time PCR analysis demonstrated that the administration of AMC and AAC down-regulated the expression of Bcl-2, Bcl-xL, while on the other hand, up-regulated Bax, Cytochrome c, caspase-9 and caspase-3 mRNA level of the S180 ascites tumor cells. 7-amino-4-methylcoumarin 76-79 caspase 9 Mus musculus 193-202 21659556-5 2011 Nevertheless, as demonstrated in caspase-9-deficient murine embryonic fibroblasts, human lymphoma cells, and chicken DT40 cells, staurosporine-induced apoptosis was essentially mediated by caspase-9. Staurosporine 129-142 caspase 9 Mus musculus 33-42 22540007-5 2012 Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Abeta(1-42) exposure. UNII-042A8N37WH 158-163 caspase 9 Mus musculus 109-118 22681485-10 2012 The expression of Bax, caspase-9, and caspase-3 in cisplatin-treated cells were also decreased by PC treatment. Cisplatin 51-60 caspase 9 Mus musculus 23-32 22056370-3 2011 In addition, an up-regulation of Bax/Bcl2 ratio with a drop in DeltaPsim and an increase of cleaved caspase 9 and 3 was found, suggesting that the alkylphenol induced osteoblast death via the mitochondrial-dependent apoptotic pathway. alkylphenol 147-158 caspase 9 Mus musculus 100-115 22098422-8 2011 Staurosporine induction of caspase 9 activity was also suppressed. Staurosporine 0-13 caspase 9 Mus musculus 27-36 21552152-9 2011 Exposure of myoblasts and myotubes for 48 and 72 h at high salmeterol concentrations induced apoptosis by the activation of the intrinsic apoptotic pathway, as confirmed by the modulation of the apoptotic proteins Bcl-xL, caspase-9, and poly (ADP-ribose) polymerase and by the cytoplasmic release of Smac/DIABLO. Salmeterol Xinafoate 59-69 caspase 9 Mus musculus 222-231 21846476-4 2011 Treatment of mesencephalic dopaminergic neuronal N27 cells with 6-OHDA (100 muM) for 24h significantly reduced mitochondrial activity and increased cytosolic cytochrome c, followed by sequential activation of caspase-9 and caspase-3. Oxidopamine 64-70 caspase 9 Mus musculus 209-218 21687940-4 2011 Icariin caused a dose-dependent decrease in the viability of MLTC-1 cells, which coincided with an increase in cell apoptosis through regulation of the expression of Bcl-2/Bax and cytochrome c, activation of caspase-9 and -3. icariin 0-7 caspase 9 Mus musculus 208-224 21617871-8 2011 TMZ (250 microM) increased the level of caspase-3/7 by 6-fold, caspase-9 by 7-fold and caspase-8 by 3-fold after a 24-h incubation, while it attenuated Bcl-2 expression (P<0.001 vs. control) and raised the proteolysis of PARP. Temozolomide 0-3 caspase 9 Mus musculus 63-72 21550109-6 2011 Furthermore, mitochondrial targeting resveratrol liposomes induced apoptosis of both non-resistant and resistant cancer cells by dissipating mitochondria membrane potential, releasing cytochrome c and increasing the activities of caspase 9 and 3. Resveratrol 37-48 caspase 9 Mus musculus 230-245 21569765-3 2011 Although caspase 8 was not activated, astin C treatment led to the cleavage of caspase 9 and caspase 3, the upregulation of Bad protein expression as well as release of cytochrome c in activated T cells. astin C 38-45 caspase 9 Mus musculus 79-88 21649480-4 2011 The proapoptotic genes, p53, Bax, caspase-9, and caspase-3, were upregulated in vernolide-A-treated cells, whereas the antiapoptotic gene, Bcl-2, was downregulated. vernolide-A 80-91 caspase 9 Mus musculus 34-43 21710101-5 2011 Taurine (1, 5, or 10 mM) also reduced cytochrome c release and inhibited activation of caspase-3 and -9, which were measured using fluorogenic substrates for caspase-3/caspase-9, in serum-deprived MC3T3-E1 cells. Taurine 0-7 caspase 9 Mus musculus 168-177 21538932-8 2011 Furthermore, DEX treatment increased the activity of caspase-9 and caspase-3. Dexamethasone 13-16 caspase 9 Mus musculus 53-62 21309636-8 2011 The activities of caspase-3/7, caspase-8 and caspase-9 were maximally seen at 12-h after exposure to DHART. artenimol 101-106 caspase 9 Mus musculus 45-54 21737642-6 2011 Results from Western blotting indicated that etomidate enhanced the levels of cytochrome c, apoptosis-inducing factor (AIF), endonuclease G (Endo G), caspase-9, caspase-3 active form and Bax proteins, but it inhibited the expression of Bcl-xl, leading to apoptosis. Etomidate 45-54 caspase 9 Mus musculus 150-159 21309636-10 2011 A relatively higher activity of caspase-8 to that of caspase-9 and the inhibition of caspsase-3/7 activity by C8I suggest that DHART induces caspase-8-mediated apoptosis involving the extrinsic pathway. artenimol 127-132 caspase 9 Mus musculus 53-62 21481001-8 2011 A higher apoptosis rate and caspase-9 in MEPM cells were detected in the ATRA group than in the control or the ATRA+FA group. Tretinoin 73-77 caspase 9 Mus musculus 28-37 21420465-6 2011 Signal transduction studies revealed that Cd markedly increased the levels of caspase-9, -8, -3, Fas and Bid, decreased mitochondrial membrane potential, enhanced cytochrome c release in the cytosol, disturbed the Bcl-2 family protein balance, cleaved PARP protein and ultimately led to apoptotic cell death. Cadmium 42-44 caspase 9 Mus musculus 78-87 21216964-8 2011 Rotenone-induced downstream activation of caspase-3 and caspase-9 were also inhibited in the neurons lacking caspase-2. Rotenone 0-8 caspase 9 Mus musculus 56-65 21845865-5 2011 Allopregnanolone inhibited the NMDA-induced apoptosis and decreased the level of active-PARP, active-caspase-3 and active-caspase-9 notably at a final concentration of 5 x 10(6) mol/L. Pregnanolone 0-16 caspase 9 Mus musculus 122-131 20951131-7 2011 Moreover, crocetin inhibited the enzymatic activity of caspase-9 in a cell-free system. crocetin 10-18 caspase 9 Mus musculus 55-64 20964710-8 2011 Silymarin/melatonin attenuated the increases in lipid peroxidation, number of degenerating neurons, nitrite content, mRNA expressions of cytochrome P-450 2E1 (CYP2E1) and GSTA4-4, catalytic activities of CYP2E1 and GST and P-p53, Bax and caspase 9 protein expressions. Silymarin 0-9 caspase 9 Mus musculus 238-247 20964710-8 2011 Silymarin/melatonin attenuated the increases in lipid peroxidation, number of degenerating neurons, nitrite content, mRNA expressions of cytochrome P-450 2E1 (CYP2E1) and GSTA4-4, catalytic activities of CYP2E1 and GST and P-p53, Bax and caspase 9 protein expressions. Melatonin 10-19 caspase 9 Mus musculus 238-247 20805790-5 2011 Both FASN inhibitors, cerulenin and orlistat, significantly reduced melanoma cell proliferation and activated the intrinsic pathway of apoptosis, as demonstrated by the cytochrome c release and caspase-9 and -3 activation. Cerulenin 22-31 caspase 9 Mus musculus 194-210 20805790-5 2011 Both FASN inhibitors, cerulenin and orlistat, significantly reduced melanoma cell proliferation and activated the intrinsic pathway of apoptosis, as demonstrated by the cytochrome c release and caspase-9 and -3 activation. Orlistat 36-44 caspase 9 Mus musculus 194-210 21471712-5 2011 The deltonin treatment caused a noticeable apoptosis in tumor tissue, which associated with increased levels of Bax, activated caspase-3, caspase-9, and cleaved poly (ADPribose) polymerase, decreased pro-caspase-8, pro-caspase-9, Bcl-2 expression levels and extracellular signal-regulated kinase-1/2 activity; and dose-dependently inhibit angiogenesis. deltonin 4-12 caspase 9 Mus musculus 138-147 21471712-5 2011 The deltonin treatment caused a noticeable apoptosis in tumor tissue, which associated with increased levels of Bax, activated caspase-3, caspase-9, and cleaved poly (ADPribose) polymerase, decreased pro-caspase-8, pro-caspase-9, Bcl-2 expression levels and extracellular signal-regulated kinase-1/2 activity; and dose-dependently inhibit angiogenesis. deltonin 4-12 caspase 9 Mus musculus 219-228 19131393-0 2011 Cordycepin Induced MA-10 Mouse Leydig Tumor Cell Apoptosis through Caspase-9 Pathway. cordycepin 0-10 caspase 9 Mus musculus 67-76 20951131-0 2011 Crocetin prevents retinal degeneration induced by oxidative and endoplasmic reticulum stresses via inhibition of caspase activity. crocetin 0-8 caspase 9 Mus musculus 113-120 19131393-8 2011 In conclusion, cordycepin induced apoptosis in MA-10 mouse Leydig tumor cells through a caspase-9 and -3 and -7 dependent pathway. cordycepin 15-25 caspase 9 Mus musculus 88-104 22174665-11 2011 The protective effect of CoQ10 was associated with reduction in superoxide production, normalization of mitochondrial membrane potential and inhibition of caspase-9 and caspase-3 activation. coenzyme Q10 25-30 caspase 9 Mus musculus 155-164 21609313-4 2011 The apoptotic genes p53, BAX, caspase-9, and caspase-3 were found upregulated in oleanolic acid-treated cells, whereas the antiapoptotic gene Bcl-2 was downregulated. Oleanolic Acid 81-95 caspase 9 Mus musculus 30-39 21611191-6 2011 In primary thymocytes, Casp9DN delayed dexamethasone (Dex)-induced cell death, altered mitochondrial structure, and decreased oxidant production. Dexamethasone 39-52 caspase 9 Mus musculus 23-28 21611191-6 2011 In primary thymocytes, Casp9DN delayed dexamethasone (Dex)-induced cell death, altered mitochondrial structure, and decreased oxidant production. Dexamethasone 54-57 caspase 9 Mus musculus 23-28 20591973-8 2010 After treatment with calcitriol and KTZ/Dex, although caspase-9 and caspase-3 were not activated and cytochrome c was not released by mitochondria, caspase-8 was activated and the truncated Bid protein level was increased. Calcitriol 21-31 caspase 9 Mus musculus 54-63 20813173-11 2010 In addition, pubertal BPA exposure upregulated the level of Bax and active caspase-9 in testes. bisphenol A 22-25 caspase 9 Mus musculus 75-84 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. ho-12h 35-41 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. hvho 42-46 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. Deuterium 39-41 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. 4h 55-57 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. ho-12h 124-130 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. hvho 131-135 caspase 9 Mus musculus 0-9 20833778-9 2010 Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. 4h 136-138 caspase 9 Mus musculus 0-9 20591973-8 2010 After treatment with calcitriol and KTZ/Dex, although caspase-9 and caspase-3 were not activated and cytochrome c was not released by mitochondria, caspase-8 was activated and the truncated Bid protein level was increased. Ketoconazole 36-39 caspase 9 Mus musculus 54-63 20498252-8 2010 Antisense suppression of GADD45alpha expression significantly reduced sulindac and indomethacin-induced activation of caspase-9 and apoptosis in AGS cells. Indomethacin 83-95 caspase 9 Mus musculus 118-127 21141502-6 2010 RESULT: Average optical density analysis indicated that, compared to the normal group, 0.03 mmol x L(-1) gentamycin could significantly activate Caspase-9 and Caspase-3, downregulate the ratio of Bcl-2 and Bax protein expression. Gentamicins 105-115 caspase 9 Mus musculus 145-154 21141502-7 2010 Compared to the gentamycin model group, ELZC pills significantly inhibited the enzymatic activity of Caspase-9 and upregulated the ratio of Bcl-2 and Bax protein expression, showing inhibition trend toward the enzymatic activity of Caspase-3. Gentamicins 16-26 caspase 9 Mus musculus 101-110 20116082-7 2010 Our results indicate that the ultrasonically activated Hp can cause obvious cell apoptosis (AI, 57.66%) at 3h after treatment, and this effect can be significantly reduced by caspase-9 inhibitor (AI, 20.76%) and the oxygen scavenger NaN(3) (20.11%). Hematoporphyrins 55-57 caspase 9 Mus musculus 175-184 20012353-9 2010 Apoptosis-inducing factor (Aif) expression was increased in DPN-treated tumors, while active caspase 9 was up-regulated in PPT-treated mice, demonstrating the involvement of the intrinsic apoptotic pathway in estrogen-induced regression in this model. 4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol 123-126 caspase 9 Mus musculus 93-102 20116082-7 2010 Our results indicate that the ultrasonically activated Hp can cause obvious cell apoptosis (AI, 57.66%) at 3h after treatment, and this effect can be significantly reduced by caspase-9 inhibitor (AI, 20.76%) and the oxygen scavenger NaN(3) (20.11%). Sodium Azide 233-239 caspase 9 Mus musculus 175-184 20116082-10 2010 In comparison with the control cells, the SDT-treated cells showed obvious cytochrome-c and Bax translocations, caspase activation, Bax expression, and PARP cleavage at 1h after SDT-treatment. 3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione 42-45 caspase 9 Mus musculus 112-119 19948164-7 2010 Furthermore, dexamethasone treatment induced cortex and hippocampus neuron apoptosis as well as increasing the activity of caspase-9 and caspase-3. Dexamethasone 13-26 caspase 9 Mus musculus 123-132 19759125-7 2010 The apoptotic effect of MK801-induced BAX expression, mitochondrial potential collapse and caspase-9 activation. Dizocilpine Maleate 24-29 caspase 9 Mus musculus 91-100 19759125-8 2010 In vivo Bax small interfering ribonucleic acid and a caspase-9 inhibitor abrogated MK801-induced apoptosis and pyknotic nucleus formation. Dizocilpine Maleate 83-88 caspase 9 Mus musculus 53-62 20007710-5 2010 Here we show for the first time that treatment with 2% isoflurane for 6 h can increase pro-apoptotic factor Bax levels, decrease anti-apoptotic factor Bcl-2 levels, increase ROS accumulation, facilitate cytochrome c release from the mitochondria to the cytosol, induce activation of caspase-9 and caspase-3, and finally cause apoptosis as compared with the control condition. Isoflurane 55-65 caspase 9 Mus musculus 283-292 20193259-15 2010 Both RPM and DOC significantly increased the caspase activity in a dosage-dependent manner. Sirolimus 5-8 caspase 9 Mus musculus 45-52 20193259-15 2010 Both RPM and DOC significantly increased the caspase activity in a dosage-dependent manner. Docetaxel 13-16 caspase 9 Mus musculus 45-52 20193259-22 2010 RPM enhanced the DOC-induced upregulation of caspase activity, resulting in an increasing number of cells in sub-G1 phases. Sirolimus 0-3 caspase 9 Mus musculus 45-52 20193259-22 2010 RPM enhanced the DOC-induced upregulation of caspase activity, resulting in an increasing number of cells in sub-G1 phases. Docetaxel 17-20 caspase 9 Mus musculus 45-52 19900555-2 2010 CBD reduced acute (LDH efflux to the incubation medium) and apoptotic (caspase-9 concentration in tissue) HI brain damage by reducing glutamate and IL-6 concentration, and TNFalpha, COX-2, and iNOS expression. Glutamic Acid 134-143 caspase 9 Mus musculus 71-80 19739150-8 2010 CONCLUSIONS: Taken together, these findings suggest that in MEMM cells arsenate-mediated oxidative injury acts as an early and upstream initiator of the cell death cascade, triggering cytotoxicity, mitochondrial dysfunction, altered Bcl/Bax protein ratios, and activation of caspase-9. arsenic acid 71-79 caspase 9 Mus musculus 275-284 19853019-6 2009 In addition, the DETA/NO-triggered alteration of mitochondrial membrane permeability, cleavage of caspase-9/3, and expression of pro-apoptotic Bcl-2 family members noxa and puma occurred in wild type NPCs but not in p53 knockout NPCs. DEET 17-21 caspase 9 Mus musculus 98-109 20932246-0 2010 Diallyl disulfide induces caspase-dependent apoptosis via mitochondria-mediated intrinsic pathway in B16F-10 melanoma cells by up-regulating p53, caspase-3 and down-regulating pro-inflammatory cytokines and nuclear factor-kappabeta-mediated Bcl-2 activation. diallyl disulfide 0-17 caspase 9 Mus musculus 26-33 20932246-5 2010 DADS treatment also down-reguated Bcl-2 expression and up-regulated p53, caspase-9, and caspase-3 expression in B16F-10 melanoma cells. diallyl disulfide 0-4 caspase 9 Mus musculus 73-82 20932246-7 2010 DADS induces caspase-dependent apoptosis through a mitochondria-mediated intrinsic pathway in B16F-10 melanoma cells by activating p53 and caspase-3 gene expression and suppressing pro-inflammatory cytokines and NF-B-mediated Bcl-2 activation. diallyl disulfide 0-4 caspase 9 Mus musculus 13-20 19666099-5 2009 SB 216763 or LiCl treatments inhibited cisplatin-induced apoptosis in a dose-dependent manner and activated caspase-9, -8 and -3. SB 216763 0-9 caspase 9 Mus musculus 108-128 19666099-5 2009 SB 216763 or LiCl treatments inhibited cisplatin-induced apoptosis in a dose-dependent manner and activated caspase-9, -8 and -3. Lithium Chloride 13-17 caspase 9 Mus musculus 108-128 20578454-1 2009 The present study investigated the effect of curcumin, a phenolic compound with yellow color from Curcuma longa L., on the expression of the apoptosis-related genes [BAX (Bcl-2 associated protein X), PKB, p53, MDM2 (mouse double minute 2), caspase 9, c-Ski, smad1 and smad4] in hamster opisthorchiasis. Curcumin 45-53 caspase 9 Mus musculus 240-249 19681042-8 2009 By 8 days in culture, an increase caspase-9 activation and apoptosis of hypertrophic chondrocytes was observed in the metatarsals cultured in 7 mM phosphate. Phosphates 147-156 caspase 9 Mus musculus 34-43 19628086-8 2009 Triptolide exposure was associated with dose-dependent increases in caspase activity and annexin staining. triptolide 0-10 caspase 9 Mus musculus 68-75 19524691-1 2009 Treatment of P388D1, a macrophage-like cell line, with staurosporine triggered apoptosis through the activation of caspase-9 and caspase-3. Staurosporine 55-68 caspase 9 Mus musculus 115-124 19961759-8 2009 The mRNA levels of caspase-9 were as follows: Cu alloy (0.532 +/- 0.041), Au alloy (0.574 +/- 0.013), the negative control (0.578 +/- 0.010), Co-Cr alloy (0.617 +/- 0.009), Ag-Pd alloy (0.703 +/- 0.018), and Ni-Cr alloy (0.811 +/- 0.037). co-cr 142-147 caspase 9 Mus musculus 19-28 19961759-8 2009 The mRNA levels of caspase-9 were as follows: Cu alloy (0.532 +/- 0.041), Au alloy (0.574 +/- 0.013), the negative control (0.578 +/- 0.010), Co-Cr alloy (0.617 +/- 0.009), Ag-Pd alloy (0.703 +/- 0.018), and Ni-Cr alloy (0.811 +/- 0.037). ag-pd 173-178 caspase 9 Mus musculus 19-28 19961759-8 2009 The mRNA levels of caspase-9 were as follows: Cu alloy (0.532 +/- 0.041), Au alloy (0.574 +/- 0.013), the negative control (0.578 +/- 0.010), Co-Cr alloy (0.617 +/- 0.009), Ag-Pd alloy (0.703 +/- 0.018), and Ni-Cr alloy (0.811 +/- 0.037). ni-cr 208-213 caspase 9 Mus musculus 19-28 19393233-5 2009 Feeding of this synthetic coumarin induced positive modulations in expression of all biomarkers in DMBA administered mice, giving clues on its possible signaling pathway(s) - primarily through down-regulation of Aryl hydrocarbon receptor and PCNA and up-regulation of apoptotic proteins like Bax, Bad, Cytochrome c, Apaf, Caspase-3 and Caspase-9, resulting in an appreciable reduction in growth of papilloma in mice. coumarin 26-34 caspase 9 Mus musculus 336-345 19393233-5 2009 Feeding of this synthetic coumarin induced positive modulations in expression of all biomarkers in DMBA administered mice, giving clues on its possible signaling pathway(s) - primarily through down-regulation of Aryl hydrocarbon receptor and PCNA and up-regulation of apoptotic proteins like Bax, Bad, Cytochrome c, Apaf, Caspase-3 and Caspase-9, resulting in an appreciable reduction in growth of papilloma in mice. 6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene 99-103 caspase 9 Mus musculus 336-345 19614980-11 2009 Furthermore, blockade of caspase-9 activity with Z-LEHD-FMK prevented L-glutamine-triggered apoptosis. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 49-59 caspase 9 Mus musculus 25-34 19614980-11 2009 Furthermore, blockade of caspase-9 activity with Z-LEHD-FMK prevented L-glutamine-triggered apoptosis. Glutamine 70-81 caspase 9 Mus musculus 25-34 19614980-12 2009 Taken together, our results indicate that hydrolysis of l-glutamine and, accordingly, accumulation of ammonium in mitochondria induce the intrinsic pathway of apoptosis, characterized by mitochondrial dysfunction and activation of caspase-9, which activates caspase-3. Glutamine 56-67 caspase 9 Mus musculus 231-240 19614980-12 2009 Taken together, our results indicate that hydrolysis of l-glutamine and, accordingly, accumulation of ammonium in mitochondria induce the intrinsic pathway of apoptosis, characterized by mitochondrial dysfunction and activation of caspase-9, which activates caspase-3. Ammonium Compounds 102-110 caspase 9 Mus musculus 231-240 19431040-3 2009 We also found that PS increased the ratio of Bax/Bcl-2 and activated caspase-9 and caspase-3 but not caspase-8. Polysaccharides 19-21 caspase 9 Mus musculus 69-78 18443897-4 2009 In addition, L-carnitine treatment regulated mitochondria-dependent apoptosis pathways by inducing the up-regulation of caspase-9 and caspase-3 and the down-regulation of Bcl-2 in hepa1c1c 7 cells. Carnitine 13-24 caspase 9 Mus musculus 120-129 19379509-16 2009 (h) The BzATP-induced apoptosis could be blocked by co-treatment with inhibitors of caspase-9 and caspase-3, but not of caspase-8. 3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate 8-13 caspase 9 Mus musculus 84-93 19209030-9 2009 In the cultured cells, DHA inhibited cell viability, downregulated the expression of proliferating cell nuclear antigen and cyclin D1, and upregulated p21(WAF1/CIP1); and induced apoptosis by reducing the ratio of Bcl-2/Bax and increasing the activation of caspase-9, in a dose-dependent manner. artenimol 23-26 caspase 9 Mus musculus 257-266 19190118-6 2009 MCHB binds DNA; at nonlethal concentration, it causes cell accumulation in the S phase, and at lethal dose, it induces cell surface Annexin V and caspase-3 and caspase-9 activities. mchb 0-4 caspase 9 Mus musculus 160-169 19035350-5 2008 The inhibition of caspase activity by Z-VAD-fmk accelerated the transition from metaphase I to metaphase II, and caspase-9 and caspase-3 were detected along the meiotic spindle. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 38-47 caspase 9 Mus musculus 80-122 18253697-10 2009 Furthermore, the suppressive effects of P on cytochrome c release and caspase-9 and caspase-3 activation in serum-deprived MC3T3-E1 cells were also reversed by RU486. Mifepristone 160-165 caspase 9 Mus musculus 70-79 19082730-4 2009 MATERIALS METHODS AND RESULTS: Menadione synergized NaAsO(2) to significantly increase ROS generation and facilitate the major apoptotic signaling events: alteration of mitochondrial membrane potential, cytochrome c release and anti-apoptotic protein Bcl-2 down-regulation and subsequent activation of caspase-9 and caspase-3 followed by poly-ADP-ribose polymerase-1 cleavage. Vitamin K 3 31-40 caspase 9 Mus musculus 302-311 19081073-5 2008 We demonstrate that DYRK1A phosphorylates caspase-9 on threonine residue 125, and that this phosphorylation event is crucial to protect retina cells from apoptotic cell death. Threonine 55-64 caspase 9 Mus musculus 42-51 18617322-0 2008 Mitochondria-cytochrome C-caspase-9 cascade mediates isorhamnetin-induced apoptosis. 3-methylquercetin 53-65 caspase 9 Mus musculus 26-35 18621044-7 2008 Additionally, significant reduction of mitochondrial dependent apoptosis was observed in brain of NZB/W F1 mice treated with cystamine as compared to control group by increasing BCL-2 and reducing caspase-9, Bad, and Apaf-1 expression. Cystamine 125-134 caspase 9 Mus musculus 197-206 19016762-5 2008 MB-PDT could induce intense apoptotic cell death through a series of steps beginning with the photochemical generation of reactive oxygen species that activate the caspase-9/caspase-3 apoptosis pathway. Reactive Oxygen Species 122-145 caspase 9 Mus musculus 164-173 18586292-5 2008 Furthermore, inhibitors of pan-caspase, caspase-3 and caspase-9 significantly inhibited clivorine-induced apoptosis and rescued clivorine-decreased cell viability. clivorine 88-97 caspase 9 Mus musculus 54-63 18586292-5 2008 Furthermore, inhibitors of pan-caspase, caspase-3 and caspase-9 significantly inhibited clivorine-induced apoptosis and rescued clivorine-decreased cell viability. clivorine 128-137 caspase 9 Mus musculus 54-63 18597125-3 2008 Cell cycle arrest is associated with increased levels of p21 and reduced amounts of cyclin E. RAPTA-C treatment also enhances the levels of p53, and its treatment triggers the mitochondrial apoptotic pathway, as shown by the change in Bax to Bcl-2 ratios, resulting in cytochrome c release and caspase-9 activation. dichloro(4-cymene)(1,3,5-triaza-7-phosphatricyclo(3.3.1.1)decane)ruthenium(II) 94-101 caspase 9 Mus musculus 294-303 18421310-7 2008 z-IETD-FMK, a caspase-8 inhibitor, and z-LEHD-FMK, a caspase-9 inhibitor, significantly decreased apoptosis induced by the combined treatment. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 39-49 caspase 9 Mus musculus 53-62 18467326-2 2008 Here we show that murine caspase-9 is phosphorylated by casein kinase 2 (CK2) on a serine near the site of caspase-8 cleavage. Serine 83-89 caspase 9 Mus musculus 25-34 18467326-4 2008 Similarly, CK2 modification of Ser(348) on caspase-9 appears to render the protease refractory to cleavage by active caspase-8. Serine 31-34 caspase 9 Mus musculus 43-52 18243174-3 2008 In vitro, treatment with sargaquinoic acid or sargachromenol promoted cell death and activation of caspase-3, caspase-8, caspase-9 and poly (ADP-ribose) polymerase (PARP) in a concentration-dependent manner. sargaquinoic acid 25-42 caspase 9 Mus musculus 121-163 18497877-5 2008 Oral administration of the PIs nelfinavir and ritonavir significantly inhibited photoreceptor apoptosis, while preventing the translocation of AIF from mitochondria to the nucleus as well as the activation of caspase-9. Nelfinavir 31-41 caspase 9 Mus musculus 209-218 18497877-5 2008 Oral administration of the PIs nelfinavir and ritonavir significantly inhibited photoreceptor apoptosis, while preventing the translocation of AIF from mitochondria to the nucleus as well as the activation of caspase-9. Ritonavir 46-55 caspase 9 Mus musculus 209-218 18497877-7 2008 Nelfinavir attenuated apoptosis as well as mitochondrial release of AIF and cytochrome c, and subsequent activation of caspase-9 in vitro, in photoreceptor cultures exposed to starvation or monocyte chemoattractant protein-1-stimulated (MCP-1-stimulated) macrophages. Nelfinavir 0-10 caspase 9 Mus musculus 119-128 18243174-3 2008 In vitro, treatment with sargaquinoic acid or sargachromenol promoted cell death and activation of caspase-3, caspase-8, caspase-9 and poly (ADP-ribose) polymerase (PARP) in a concentration-dependent manner. sargachromenol 46-60 caspase 9 Mus musculus 121-163 18507048-1 2008 Hydroquinone, an activator of caspase-9 activity via reactive oxygen species, and farnesol, a post-translational down-regulator of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity suppress the growth of murine 816 melanoma cells. hydroquinone 0-12 caspase 9 Mus musculus 30-39 18380009-5 2008 Experiments with the embryonic stem cell line, ESC-B5, disclose that CTN induces apoptosis via several mechanisms, including ROS generation, increased cytoplasmic free calcium levels, intracellular nitric oxide production, enhanced Bax/Bcl-2 ratio, loss of mitochondrial membrane potential, cytochrome c release, activation of caspase-9 and caspase-3, and p21-activated protein kinase 2 and c-Jun N-terminal protein kinase activation. Citrinin 69-72 caspase 9 Mus musculus 327-336 17559077-3 2008 Furthermore, we demonstrated that PGF2alpha caused a decrement of the active caspases 9 and 3. Dinoprost 34-43 caspase 9 Mus musculus 77-93 18033239-2 2008 PGI2 overexpression protected these cells from gentamicin-induced apoptosis by reducing cleaved caspase-3 and caspase-9, cytochrome c, and decreasing generation of reactive oxygen species. Gentamicins 47-57 caspase 9 Mus musculus 110-119 17297564-0 2008 Taurine reduces caspase-8 and caspase-9 expression induced by ischemia in the mouse hypothalamic nuclei. Taurine 0-7 caspase 9 Mus musculus 30-39 17297564-8 2008 Addition of taurine (20 mM) to the incubation medium induced a marked decrease in caspase-8 and caspase-9 immunoreactivity after ischemia in SON and PVN when compared with the taurine-untreated "ischemic" group. Taurine 12-19 caspase 9 Mus musculus 96-105 17297564-9 2008 Taurine reduces ischemia-induced caspase-8 and caspase-9 expression, the key inductors of apoptosis in SON and PVN. Taurine 0-7 caspase 9 Mus musculus 47-56 19706975-5 2008 This combination markedly induced intracellular levels of reactive oxygen species (ROS) starting at 6 h and significantly decreased the mitochondrial potential starting at 12 h. The combination significantly elevated caspase-9 and caspase-3 activities at 24 and 48 h. The combination also induced hypomethylation (at 24 and 48 h), as indicated by significantly decreased 5-methyldeoxycytidine levels and SAM/SAH ratios. Reactive Oxygen Species 58-81 caspase 9 Mus musculus 217-226 19706975-5 2008 This combination markedly induced intracellular levels of reactive oxygen species (ROS) starting at 6 h and significantly decreased the mitochondrial potential starting at 12 h. The combination significantly elevated caspase-9 and caspase-3 activities at 24 and 48 h. The combination also induced hypomethylation (at 24 and 48 h), as indicated by significantly decreased 5-methyldeoxycytidine levels and SAM/SAH ratios. Reactive Oxygen Species 83-86 caspase 9 Mus musculus 217-226 17823781-6 2008 The FAAH inhibitor N-arachidonoylserotonin increased colon endocannabinoid levels, reduced ACF formation, and partially normalized cleaved caspase-3 (but not caspase-9) expression. arachidonoylserotonin 19-42 caspase 9 Mus musculus 158-167 17950979-5 2007 In an in vitro cell-based assay, we further found that ethanol increases the production of reactive oxygen species in ESC-B5 embryonic stem cells, leading to an increase in the intracellular concentrations of cytoplasmic free Ca(2+) and NO, loss of mitochondrial membrane potential, mitochondrial release of cytochrome c, activation of caspase-9 and -3, and apoptosis. Ethanol 55-62 caspase 9 Mus musculus 336-352 17950979-5 2007 In an in vitro cell-based assay, we further found that ethanol increases the production of reactive oxygen species in ESC-B5 embryonic stem cells, leading to an increase in the intracellular concentrations of cytoplasmic free Ca(2+) and NO, loss of mitochondrial membrane potential, mitochondrial release of cytochrome c, activation of caspase-9 and -3, and apoptosis. Reactive Oxygen Species 91-114 caspase 9 Mus musculus 336-352 17713842-5 2007 When the cells were treated with Alternol, chromatin condensation and phosphatidylserine externalization were observed with the down-regulation of the pro-survival gene Bcl-2 and the activation of caspase-3, caspase-9, but not caspase-8. Alternol 33-41 caspase 9 Mus musculus 208-217 17872969-8 2007 In addition, resveratrol-induced apoptosis in primary T cells correlated with cleavage of caspase-8, caspase-9, caspase-3, poly(ADP-ribose) polymerase, and release of cytochrome c. Data from the present study demonstrate, for the first time, the ability of resveratrol to trigger apoptosis in activated T cells and its potential use in the treatment of inflammatory and autoimmune diseases including, MS. Resveratrol 13-24 caspase 9 Mus musculus 101-110 18030663-6 2007 Results of western blot analysis showed that [6]-gingerol upregulated the testosterone depleted levels of p53 in mouse prostate and upregulated its downstream regulator Bax and further activated Caspase-9 and Caspase-3 in both LNCaP cells and in mouse prostate. gingerol 45-57 caspase 9 Mus musculus 195-204 17895242-3 2007 In vitro studies using the murine dopaminergic cell line MN9D showed that leptin attenuated 6-OHDA-induced apoptotic markers, including caspase-9 and caspase-3 activation, internucleosomal DNA fragmentation, and cytochrome c release. Oxidopamine 92-98 caspase 9 Mus musculus 136-145 17277231-3 2007 Curcumin treatment resulted an increase in the protein levels of both Bax and Bak, and mitochondrial translocation and activation of Bax in MEFs to trigger drop in mitochondrial membrane potential, cytosolic release of apoptogenic molecules [cytochrome c and second mitochondria-derived activator of caspases (Smac)/direct inhibitor of apoptosis protein-binding protein with low isoelectric point], activation of caspase-9 and caspase-3 and ultimately apoptosis. Curcumin 0-8 caspase 9 Mus musculus 413-422 17481927-0 2007 Stobadine inhibits doxorubicin-induced apoptosis through a caspase-9 dependent pathway in P815 mastocytoma cells. dicarbine 0-9 caspase 9 Mus musculus 59-68 17481927-0 2007 Stobadine inhibits doxorubicin-induced apoptosis through a caspase-9 dependent pathway in P815 mastocytoma cells. Doxorubicin 19-30 caspase 9 Mus musculus 59-68 17481927-4 2007 In the present study we investigated the effects of stobadine, a pyridoindole antioxidant in a DOXO-induced apoptosis model of P815 cells by flow cytometric analyses and by measuring caspase-3 and caspase-9 activities. dicarbine 52-61 caspase 9 Mus musculus 197-206 17481927-7 2007 The antiapoptotic effect of stobadine was further confirmed by inhibition of caspase-3 and caspase-9 activities. dicarbine 28-37 caspase 9 Mus musculus 91-100 17569628-3 2007 EGCG caused growth arrest at G1 stage of cell cycle through regulation of cyclin D1, cdk4, cdk6, p21/WAF1/CIP1 and p27/KIP1, and induced apoptosis through generation of reactive oxygen species and activation of caspase-3 and caspase-9. epigallocatechin gallate 0-4 caspase 9 Mus musculus 225-234 17277231-4 2007 Furthermore, MEFs derived from Bax and Bak double-knockout (DKO) mice exhibited even greater protection against curcumin-induced release of cytochrome c and Smac, activation of caspase-3 and caspase-9 and induction of apoptosis compared with wild-type MEFs or single-knockout Bax(-/-) or Bak(-/-) MEFs. Curcumin 112-120 caspase 9 Mus musculus 191-200 17130845-8 2007 When caspase-9-deficient mouse embryonic fibroblasts (MEFs) were treated with staurosporine, WTS was proteolysed by activated endogenous Omi without induction of cell death. Staurosporine 78-91 caspase 9 Mus musculus 5-14 17403866-2 2007 In the cells treated with z-VAD-fmk, activation of caspase-8, caspase-3/7, and caspase-9 was clearly suppressed, and DNA fragmentation of the infected cells was also reduced. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 26-35 caspase 9 Mus musculus 79-88 17403866-7 2007 Among inhibitors specific for each caspase, only the caspase-9-specific inhibitor enhanced the generation of ROS and induced necrosis of the infected cells. Reactive Oxygen Species 109-112 caspase 9 Mus musculus 35-42 17403866-7 2007 Among inhibitors specific for each caspase, only the caspase-9-specific inhibitor enhanced the generation of ROS and induced necrosis of the infected cells. Reactive Oxygen Species 109-112 caspase 9 Mus musculus 53-62 17403866-10 2007 These results indicated that caspase-9, which was activated by infection with virulent M. tuberculosis, contributed to the inhibition of necrosis of the infected host cells, presumably through suppression of intracellular ROS generation. Reactive Oxygen Species 222-225 caspase 9 Mus musculus 29-38 17311288-6 2007 In Lewis lung carcinoma (LLC) cells, OXO not only induces S-phase arrest and mitochondria/caspase-9 pathway mediated apoptosis, but also effectively down-regulated the hypoxia-induced expression of HIF-1alpha and VEGF at mRNA and protein levels in LLC and decreased VEGF secretion into conditioned culture media. 6-(1-oxobutyl)-5,8-dimethoxy-1,4-naphthoquinone 37-40 caspase 9 Mus musculus 90-99 17360717-12 2007 These results suggest that, in P-815 cells, histamine synthesis is augmented through the post-translational cleavage of HDC, which is mediated by caspase-9. Histamine 44-53 caspase 9 Mus musculus 146-155 17265069-9 2007 The identification of the germ-cell apoptotic pathway induced after testicular IR, including the key players in the pathway subsequent to ROS (BAX, caspase 9, and caspase 2), aids our understanding of IR injury in the testis and provides a wider background for the development of therapeutic interventions to rescue testis function. Reactive Oxygen Species 138-141 caspase 9 Mus musculus 148-157 17498489-11 2007 SP method was also used to detect the expressions of cleaved caspase-3, caspase-8 and caspase-9. TFF2 protein, human 0-2 caspase 9 Mus musculus 86-95 17300814-7 2007 In support of the role of JNK in promoting the mitochondria-mediated apoptosis pathway, SP600125 prevented cytochrome c release, caspase-9 and caspase-3 activity. pyrazolanthrone 88-96 caspase 9 Mus musculus 129-138 16880202-7 2006 Finally, we have shown that aspirin treatment caused changes in the mitochondrial membrane potential, release of cytochrome c from mitochondria, and activation of caspase-9 and -3, which could be because of the proteasomal dysfunction. Aspirin 28-35 caspase 9 Mus musculus 163-179 17207636-4 2007 Administration of phenyl-N-tert-butylnitrone (PBN), a potent ROS scavenger, reduced the development of thermal hyperalgesia and mechanical allodynia at 1 and 3 days post-CCI, and decreased the mRNA levels of bax, apaf-1, and caspase-9. phenyl-N-tert-butylnitrone 18-44 caspase 9 Mus musculus 225-234 17207636-4 2007 Administration of phenyl-N-tert-butylnitrone (PBN), a potent ROS scavenger, reduced the development of thermal hyperalgesia and mechanical allodynia at 1 and 3 days post-CCI, and decreased the mRNA levels of bax, apaf-1, and caspase-9. phenyl-N-tert-butylnitrone 46-49 caspase 9 Mus musculus 225-234 17135272-6 2007 Likewise, carbon monoxide, at low concentrations, markedly inhibited hyperoxia-induced endothelial cell death by inhibiting cytochrome c release and caspase-9/3 activation. Carbon Monoxide 10-25 caspase 9 Mus musculus 149-158 16675471-9 2006 Both HA- and RES-induced cleavage of caspase-9 and caspase-3 and PARP were completely blocked by a pan caspase inhibitor, Z-VAD-FMK. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 122-131 caspase 9 Mus musculus 37-46 17006946-7 2006 Our results showed that administration of indomethacin to PiZ mice resulted in increased hepatic injury, indicated by increased hepatocellular proliferation and increased activation of caspase 9. Indomethacin 42-54 caspase 9 Mus musculus 185-194 16709801-6 2006 In vitro induction of apoptosis can be inhibited by the caspase-9 inhibitor (Z-LEHD-FMK) but not by the inhibitor to caspase-8 or -10. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 77-87 caspase 9 Mus musculus 56-65 16709801-12 2006 Depletion of recovered alveolar macrophages by intranasal administration of clodronate-containing liposomes in caspase-9 inhibitor-treated animals abrogates the effects of the inhibitor. Clodronic Acid 76-86 caspase 9 Mus musculus 111-120 16621521-10 2006 However, increased caspase-3 activity by estradiol was observed in the presence of caspase-9 inhibitor, indicating the preferential involvement of caspase-8 pathway. Estradiol 41-50 caspase 9 Mus musculus 83-92 16453149-3 2006 Local injections of Z-LEHD-fmk, a specific caspase-9 inhibitor, into thymi of septic mice led to the complete inhibition of caspase-9, decreased apoptosis of resident tissue cells, and, in addition, reduced further downstream caspase-3 activity. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 20-30 caspase 9 Mus musculus 43-52 16651419-4 2006 Furthermore, PAF inhibited etoposide-induced increases in caspase-3, caspase-8, and caspase-9 activities, as well as cell death. Etoposide 27-36 caspase 9 Mus musculus 84-93 16453149-3 2006 Local injections of Z-LEHD-fmk, a specific caspase-9 inhibitor, into thymi of septic mice led to the complete inhibition of caspase-9, decreased apoptosis of resident tissue cells, and, in addition, reduced further downstream caspase-3 activity. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 20-30 caspase 9 Mus musculus 124-133 16585560-2 2006 H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. Hydrogen Peroxide 0-4 caspase 9 Mus musculus 68-77 16488414-5 2006 In contrast, only when treated with 4-HC, caspase-9 activation and the increase in the intracellular expression of Bax were detected. 4-hydroxycyclophosphamide 36-40 caspase 9 Mus musculus 42-51 16306138-5 2006 Glutathione and inhibitors of caspase-8 or caspase-9, but not of FasL, inhibited these effects, suggesting their dependence on ROS, caspase-8 and -9, in a Fas/FasL-independent pathway. Reactive Oxygen Species 127-130 caspase 9 Mus musculus 43-52 16306138-7 2006 These results demonstrate that the initial bleomycin-induced oxidative stress causes a direct apoptotic effect in lung epithelial cells involving a regulatory role of caspase-8 on caspase-9. Bleomycin 43-52 caspase 9 Mus musculus 180-189 16515545-4 2006 Treatment of the neurons with taurine, a caspase 9-specific inhibitor, could prevent the amphiphile-induced apoptotic cell death, suggesting that formation of apoptosome, followed by caspase 9 and caspase 3 activation, might play a critical role in the neuronal death pathway. Taurine 30-37 caspase 9 Mus musculus 41-50 16515545-4 2006 Treatment of the neurons with taurine, a caspase 9-specific inhibitor, could prevent the amphiphile-induced apoptotic cell death, suggesting that formation of apoptosome, followed by caspase 9 and caspase 3 activation, might play a critical role in the neuronal death pathway. Taurine 30-37 caspase 9 Mus musculus 183-192 16443586-9 2006 CS induces MA-10 cell apoptosis by activating caspase-8-dependent and caspase-9-independent pathways and downregulating NF-?B protein expression. Cesium 0-2 caspase 9 Mus musculus 70-79 16505011-8 2006 This death was caspase dependent, as shown by IHC and caspase inhibition with zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 78-86 caspase 9 Mus musculus 15-22 16505011-8 2006 This death was caspase dependent, as shown by IHC and caspase inhibition with zVAD-fmk. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 78-86 caspase 9 Mus musculus 54-61 16443586-9 2006 CS induces MA-10 cell apoptosis by activating caspase-8-dependent and caspase-9-independent pathways and downregulating NF-?B protein expression. ma-10 11-16 caspase 9 Mus musculus 70-79 16291826-3 2006 atRA-induced apoptosis is associated with activation of the initiator caspase-9 and the effector caspase-3, but not of the effector caspase-8. Tretinoin 0-4 caspase 9 Mus musculus 70-79 16420519-3 2006 The aim of this study was to investigate the effects of the caspase-9 inhibitor Ac-LEHD-CHO on tumor necrosis factor receptor (TNFR)- and Fas-mediated hepatocyte apoptosis in vivo, in order to evaluate the similarities and distinctions between TNFR- and Fas-mediated signaling pathways. acetyl-leucyl-glutamyl-histidyl-aspartal 80-91 caspase 9 Mus musculus 60-69 16420519-3 2006 The aim of this study was to investigate the effects of the caspase-9 inhibitor Ac-LEHD-CHO on tumor necrosis factor receptor (TNFR)- and Fas-mediated hepatocyte apoptosis in vivo, in order to evaluate the similarities and distinctions between TNFR- and Fas-mediated signaling pathways. ammonium ferrous sulfate 138-141 caspase 9 Mus musculus 60-69 16420519-3 2006 The aim of this study was to investigate the effects of the caspase-9 inhibitor Ac-LEHD-CHO on tumor necrosis factor receptor (TNFR)- and Fas-mediated hepatocyte apoptosis in vivo, in order to evaluate the similarities and distinctions between TNFR- and Fas-mediated signaling pathways. ammonium ferrous sulfate 254-257 caspase 9 Mus musculus 60-69 16291826-4 2006 A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 59-69 caspase 9 Mus musculus 39-48 16144541-6 2005 Administration of 0.1 microM MG132 led to activation of a mitochondria-dependent apoptotic signaling cascade involving cytochrome c, caspase-9, caspase-3 and degradation of tau protein; such activation was markedly reduced with 10 microM MG132. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 29-34 caspase 9 Mus musculus 133-142 16291826-4 2006 A broad caspase inhibitor (z-VAD-fmk), caspase-9 inhibitor z-LEHD-fmk and caspase-3 inhibitor (z-DEVD-fmk) blocked atRA-induced DNA fragmentation and sub-G1 fraction, but not caspase-8 inhibitor z-IETD-fmk. Tretinoin 115-119 caspase 9 Mus musculus 39-48 16418769-5 2005 However, the caspase-9 inhibitor (z-LEHD-fmk) only increased oridonin-induced L929 cell death. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 34-44 caspase 9 Mus musculus 13-22 16418769-5 2005 However, the caspase-9 inhibitor (z-LEHD-fmk) only increased oridonin-induced L929 cell death. oridonin 61-69 caspase 9 Mus musculus 13-22 16085184-10 2005 (3) Antisense phosphorothioate oligonucleotides against Smac/DIABLO markedly inhibited de novo synthesis of Smac/DIABLO and this effect was accompanied by decreased apoptosis and activation of caspase-3 and caspase-9 induced by H(2)O(2) (P<0.05). Phosphorothioate Oligonucleotides 14-47 caspase 9 Mus musculus 207-216 16156740-4 2005 Using the midbrain-derived MN9D dopaminergic cell line, we found that MPP+ treatment resulted in an active form of cell death that could not be prevented by caspase inhibitors or over-expression of a dominant negative inhibitor of apoptotic protease activating factor 1/caspase-9. mangion-purified polysaccharide (Candida albicans) 70-74 caspase 9 Mus musculus 270-279 15975932-5 2005 Additionally, treatment of human and murine cells with ER stress agents led to the cleavage of the caspase-4 fluorogenic substrate, LEVD-7-amino-4-trifluoromethylcoumarin, in the presence or absence of caspase-12 or caspase-4 expression, whereas Bcl-x(L) or a dominant negative caspase-9 overexpression inhibited LEVD-7-amino-4-trifluoromethylcoumarin cleavage. levd-7-amino-4-trifluoromethylcoumarin 132-170 caspase 9 Mus musculus 278-287 16081829-3 2005 In this study, we report that in murine macrophages GBS induces unique changes in the regulation and localization of the apoptotic regulators Bad, 14-3-3, and Omi/high-temperature requirement A2 and leads to the release of cytochrome c and the activation of caspase-9 and caspase-3. gbs 52-55 caspase 9 Mus musculus 258-267 16046310-9 2005 3,4-DGE results in Bax oligomerization, release of cytochrome c from mitochondria, activation of caspases-9 and -3, and Bid proteolysis. 3,4-dideoxyglucosone-3-ene 0-7 caspase 9 Mus musculus 97-114 15944155-8 2005 When the cells were treated with dexamethasone, a rapid down-regulation of AP-4 and Casp-9 was observed whether the cells were GC-sensitive lymphomas or GC-insensitive L929 fibroblast cells. Dexamethasone 33-46 caspase 9 Mus musculus 84-90 15976027-7 2005 Our studies demonstrate that normal phosphorus levels are required for growth plate maturation and implicate a critical role for phosphate-regulated apoptosis of hypertrophic chondrocytes via activation of the caspase-9-mediated mitochondrial pathway. Phosphorus 36-46 caspase 9 Mus musculus 210-219 15976027-7 2005 Our studies demonstrate that normal phosphorus levels are required for growth plate maturation and implicate a critical role for phosphate-regulated apoptosis of hypertrophic chondrocytes via activation of the caspase-9-mediated mitochondrial pathway. Phosphates 129-138 caspase 9 Mus musculus 210-219 15956254-4 2005 PCI-2000 triggers an apoptotic pathway in these tumor cells as shown by release of cytochrome c from mitochondria; activation of caspases 9, 8, and 3; cleavage of the caspase substrate poly(ADP-ribose) polymerase; and Annexin V binding. PCI 2000 0-8 caspase 9 Mus musculus 129-149 15670579-6 2005 Caspase 9 and MKP-1 genes showed distinct differences in patterns of expression between FK228-sensitive and resistant tumors and have been known to have roles in apoptosis and chromatin remodeling. romidepsin 88-93 caspase 9 Mus musculus 0-9 15778364-4 2005 In WEHI-231 cells, the natural PPARgamma agonist 15-deoxy-Delta(12,14)-PGJ(2) and the synthetic PPARgamma agonist ciglitazone induced activation of caspase 3 and caspase 9, a decrease in mitochondrial membrane potential, and caused cleavage of the caspase substrate poly(ADP-ribose) polymerase. 15-deoxy-delta( 49-64 caspase 9 Mus musculus 162-171 15778364-4 2005 In WEHI-231 cells, the natural PPARgamma agonist 15-deoxy-Delta(12,14)-PGJ(2) and the synthetic PPARgamma agonist ciglitazone induced activation of caspase 3 and caspase 9, a decrease in mitochondrial membrane potential, and caused cleavage of the caspase substrate poly(ADP-ribose) polymerase. ciglitazone 114-125 caspase 9 Mus musculus 162-171 15670579-7 2005 The expression of caspase 9 gene was higher in FK228-sensitive tumors and the expression of MKP-1 gene was higher in FK228-resistant tumors. romidepsin 47-52 caspase 9 Mus musculus 18-27 15670579-8 2005 Caspase 9 and MKP-1 genes in the other FK228-sensitive tumors had the same patterns of expression as they did in PC-3 and SC-6 tumors. romidepsin 39-44 caspase 9 Mus musculus 0-9 15670579-9 2005 Our results present profiles of gene expression related to FK228 and marker genes to predict sensitivity to FK228, such as caspase 9 and MKP-1 genes. romidepsin 108-113 caspase 9 Mus musculus 123-132 15545281-0 2005 Taurine monochloramine activates a cell death pathway involving Bax and Caspase-9. N-chlorotaurine 0-22 caspase 9 Mus musculus 72-81 15545281-9 2005 Both Bcl-2 and, to a lesser degree, the dominant negative form of caspase-9 inhibit cell death following TauNHCl treatment. taunhcl 105-112 caspase 9 Mus musculus 66-75 15749635-6 2005 Cell staining with the mitochondrial specific dye JC-1 and detection of caspase-9 activation revealed that genistein produced mitochondrial depolarization as an early step in the induction of apoptosis. Genistein 107-116 caspase 9 Mus musculus 72-81 15389638-3 2005 This process involved the activation of both caspases-9 and -3, suggesting that L-glutamine deprivation initiated an intrinsic apoptotic pathway in Sp2/0-Ag14 cells. Glutamine 80-91 caspase 9 Mus musculus 45-62 15871184-7 2005 RESULTS: H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. Hydrogen Peroxide 9-13 caspase 9 Mus musculus 50-59 15871184-7 2005 RESULTS: H2O2 ( 0.5 mmol/L ) activated caspase-3, caspase-9 8 h after the treatment and specific morphological changes of apoptosis 12 h after the treatment, and overexpression of Smac significantly promoted H2O2-induced activation of caspase-3, caspase-9 and apoptosis in C2C12 myogenic cells. Hydrogen Peroxide 9-13 caspase 9 Mus musculus 246-255 16173058-9 2005 These results demonstrate that UCB-mediated apoptosis in Hepa 1c1c7 cells is associated with increased oxidative stress and that caspase-9, and definitely not caspase-2, is the initiator caspase for apoptosis in UCB-treated Hepa 1c1c7 cells. ucb 31-34 caspase 9 Mus musculus 129-138 16173058-9 2005 These results demonstrate that UCB-mediated apoptosis in Hepa 1c1c7 cells is associated with increased oxidative stress and that caspase-9, and definitely not caspase-2, is the initiator caspase for apoptosis in UCB-treated Hepa 1c1c7 cells. ucb 212-215 caspase 9 Mus musculus 129-138 16131815-6 2005 In addition, a caspase-9 inhibitor partially attenuated this effect of H2O2. Hydrogen Peroxide 71-75 caspase 9 Mus musculus 15-24 15356125-12 2004 These data indicate that DX-induced apoptosis is mediated in part by SP, which contributes, together with proteasome activity, to caspase-8-3 processing independently of mitochondria, and in part by the proteasome/mitochondria pathway, although independently of caspase-9 activation. Sphingosine 69-71 caspase 9 Mus musculus 262-271 15544921-6 2004 The combination of emodin and arsenic promoted the major apoptotic signaling events, i.e., the collapse of the mitochondrial transmembrane potential, the release of cytochrome c, and the activation of caspases 9 and 3. Arsenic 30-37 caspase 9 Mus musculus 201-217 15516929-1 2004 Here, we report that tPA potentiates apoptosis in ischemic human brain endothelium and in mouse cortical neurons treated with N-methyl-D-aspartate (NMDA) by shifting the apoptotic pathways from caspase-9 to caspase-8, which directly activates caspase-3 without amplification through the Bid-mediated mitochondrial pathway. N-Methylaspartate 126-146 caspase 9 Mus musculus 194-203 15516929-1 2004 Here, we report that tPA potentiates apoptosis in ischemic human brain endothelium and in mouse cortical neurons treated with N-methyl-D-aspartate (NMDA) by shifting the apoptotic pathways from caspase-9 to caspase-8, which directly activates caspase-3 without amplification through the Bid-mediated mitochondrial pathway. N-Methylaspartate 148-152 caspase 9 Mus musculus 194-203 15557813-6 2004 We also observed ceramide/ DMS induced disruption of mitochondrial membrane potential (MMP) and activation of caspase- 9 and -3 in a radiation-dose-dependent manner. Ceramides 17-25 caspase 9 Mus musculus 110-127 15557813-6 2004 We also observed ceramide/ DMS induced disruption of mitochondrial membrane potential (MMP) and activation of caspase- 9 and -3 in a radiation-dose-dependent manner. dms 27-30 caspase 9 Mus musculus 110-127 15517873-0 2004 In vivo adriamycin-induced apoptosis in peritoneal murine macrophages: partial participation of a caspase cascade. Doxorubicin 8-18 caspase 9 Mus musculus 98-105 15517873-12 2004 CONCLUSION: In these experimental conditions, ADM induced AP in a mainly caspase-9-dependent manner and this was related to a reduction in the deltapsim. Doxorubicin 46-49 caspase 9 Mus musculus 73-82 15352222-0 2004 6-Hydroxydopamine induces dopaminergic cell degeneration via a caspase-9-mediated apoptotic pathway that is attenuated by caspase-9dn expression. Oxidopamine 0-17 caspase 9 Mus musculus 63-72 15352222-0 2004 6-Hydroxydopamine induces dopaminergic cell degeneration via a caspase-9-mediated apoptotic pathway that is attenuated by caspase-9dn expression. Oxidopamine 0-17 caspase 9 Mus musculus 122-131 15352222-5 2004 Finally, overexpression of a mutant caspase-9 with dominant negative phenotype (caspase-9dn) in MN9D cells and primary dopaminergic neurons via the adenovirus and adenoassociated virus gene delivery system, respectively, conferred marked increases in tolerance to the toxicity of 6-OHDA. Oxidopamine 280-286 caspase 9 Mus musculus 36-45 15352222-6 2004 These results point to the intrinsic caspase-9/caspase-3 cascade as the predominant signaling pathway underlying dopaminergic cell death induced by 6-OHDA and suggest that gene delivery of caspase-9dn can attenuate this pathway and its degenerative consequences. Oxidopamine 148-154 caspase 9 Mus musculus 37-46 15352222-6 2004 These results point to the intrinsic caspase-9/caspase-3 cascade as the predominant signaling pathway underlying dopaminergic cell death induced by 6-OHDA and suggest that gene delivery of caspase-9dn can attenuate this pathway and its degenerative consequences. Oxidopamine 148-154 caspase 9 Mus musculus 189-198 15188275-10 2004 Furthermore, Bcl-2 overexpression prevented neomycin-induced activation of caspase-9 in hair cells. Neomycin 44-52 caspase 9 Mus musculus 75-84 15180944-8 2004 Consistent with initiation of apoptosis, cellular caspase-8, caspase-9 and caspase-3 activities were elevated in lovastatin-treated cells. Lovastatin 113-123 caspase 9 Mus musculus 61-70 15180944-9 2004 The mitochondrial membrane potential was also decreased, with subsequent release of cytochrome c. However, lovastatin-induced cell death was significantly reduced by the broad spectrum caspase inhibitor z-VAD-fmk, as well as the caspase-9 inhibitor z-LEHD-fmk and the caspase-3 inhibitor z-DEVD-fmk, but not by the specific caspase-8 inhibitor z-IETD-fmk. Lovastatin 107-117 caspase 9 Mus musculus 229-238 15180944-9 2004 The mitochondrial membrane potential was also decreased, with subsequent release of cytochrome c. However, lovastatin-induced cell death was significantly reduced by the broad spectrum caspase inhibitor z-VAD-fmk, as well as the caspase-9 inhibitor z-LEHD-fmk and the caspase-3 inhibitor z-DEVD-fmk, but not by the specific caspase-8 inhibitor z-IETD-fmk. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 249-259 caspase 9 Mus musculus 229-238 15188275-3 2004 Aminoglycoside-induced hair cell death can be prevented by broad-spectrum inhibition of caspases, a family of proteases that mediate apoptotic and programmed cell death in a wide variety of systems. Aminoglycosides 0-14 caspase 9 Mus musculus 88-96 15028783-6 2004 Furthermore, caspase-9 activity was significantly increased 6 h after DCE exposure. vinylidene chloride 70-73 caspase 9 Mus musculus 13-22 15188275-4 2004 More specifically, aminoglycoside-induced hair cell death requires activation of caspase-9. Aminoglycosides 19-33 caspase 9 Mus musculus 81-90 15188275-5 2004 Caspase-9 activation requires release of mitochondrial cytochrome c into the cytoplasm, indicating that aminoglycoside-induced hair cell death is mediated by the mitochondrial (or "intrinsic") cell death pathway. Aminoglycosides 104-118 caspase 9 Mus musculus 0-9 15172982-3 2004 DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential. DETA-NO 0-7 caspase 9 Mus musculus 171-180 15056807-6 2004 MH-S cells pretreated with pepstatin A, an inhibitor of lysosomal cathepsin D, showed decreased caspase 9 and 3 activation as well as a decreased percentage of cells that became apoptotic. pepstatin 27-38 caspase 9 Mus musculus 96-111 15056807-7 2004 DNA fragmentation and caspase 9 and 3 activation were also decreased in cells pretreated with despiramine, an inhibitor of lysosomal acidic sphingomyelinase. despiramine 94-105 caspase 9 Mus musculus 22-31 15172982-3 2004 DETA-NO-treated DCs became resistant to tumor-induced apoptosis because DETA-NO prevented tumor-induced changes in the expression of Bcl-2, Bax, and Bcl-xL; activation of caspase-9; and a reduction in the mitochondrial membrane potential. DETA-NO 72-79 caspase 9 Mus musculus 171-180 15125997-6 2004 Taken together, these results demonstrated that BaP-induced apoptosis of Hepa1c1c7 cells via activation of intrinsic caspase pathway including caspase-3, caspase-9, with mitochondrial dysfunction and p53 activation. Benzo(a)pyrene 48-51 caspase 9 Mus musculus 154-163 15214581-7 2004 Finally, we showed that culture of oocytes in staurosporine increased the activity of caspase-8 and caspase-9. Staurosporine 46-59 caspase 9 Mus musculus 100-109 15108327-7 2004 We also found that TCHQ induced a change in mitochondrial transmembrane potential, and that caspase-9 and subsequent caspase-3 can be activated during TCHQ-induced acute apoptosis. tchq 151-155 caspase 9 Mus musculus 92-101 15108327-8 2004 Interestingly, TCHQ induced a significant upregulation of Bcl-2 expression, and over-expressed Bcl-2 can dramatically inhibit the change of mitochondria membrane potential and activation of both caspase-9 and -3. tchq 15-19 caspase 9 Mus musculus 195-211 15063731-3 2004 We demonstrated that cells aggregated on cellulose substrates for up to 48 h underwent programmed cell death that was associated with phosphatidylserine flipping and caspase 9 and caspase 3 activation, suggesting a mitochondria-dependent apoptotic process. Cellulose 41-50 caspase 9 Mus musculus 166-175 14701837-7 2004 Addition of curcumin to neuro 2a cells induces a rapid decrease in mitochondrial membrane potential and the release of cytochrome c into cytosol, followed by activation of caspase-9 and caspase-3. Curcumin 12-20 caspase 9 Mus musculus 172-181 14982845-9 2004 Furthermore, Z-LEHD-FMK, a caspase-9 inhibitor, but not Z-IETD-FMK, a caspase-8 inhibitor, attenuated the overload-induced apoptosis. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 13-23 caspase 9 Mus musculus 27-36 15033175-5 2004 In YAC46 MSNs, NMDA stimulated significantly higher activation of caspase-3 and caspase-9 but not caspase-8, and NMDA-induced caspase-3 and -9 activation was markedly attenuated by cyclosporin A. N-Methylaspartate 15-19 caspase 9 Mus musculus 80-89 15033175-5 2004 In YAC46 MSNs, NMDA stimulated significantly higher activation of caspase-3 and caspase-9 but not caspase-8, and NMDA-induced caspase-3 and -9 activation was markedly attenuated by cyclosporin A. Cyclosporine 181-194 caspase 9 Mus musculus 80-89 14747384-6 2004 However, paracetamol-induced apoptosis is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome c or Smac/DIABLO. Acetaminophen 9-20 caspase 9 Mus musculus 98-107 15648737-7 2004 In hypothermic conditions, Fas-mediated cytochrome c release from mitochondria of hepatocytes and the proximate downstream activation of caspase-9 were suppressed under mild hypothermic conditions. ammonium ferrous sulfate 27-30 caspase 9 Mus musculus 137-146 20021098-4 2004 Interestingly, caspase-9 inhibitor Z-LEHD-FMK blocked caspase-2 activation suggesting that caspase-2 activation is not due to death receptor activation but results from activation of other caspases that are dependent on caspase-9 such as caspase-3. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 35-45 caspase 9 Mus musculus 15-24 14971037-1 2004 In thymocytes, dexamethasone initiates cytochrome c-dependent processing of caspase-9 and the activation of caspase-3 to trigger apoptotic damage. Dexamethasone 15-28 caspase 9 Mus musculus 76-85 20021098-4 2004 Interestingly, caspase-9 inhibitor Z-LEHD-FMK blocked caspase-2 activation suggesting that caspase-2 activation is not due to death receptor activation but results from activation of other caspases that are dependent on caspase-9 such as caspase-3. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 35-45 caspase 9 Mus musculus 220-229 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 206-216 caspase 9 Mus musculus 65-74 14714619-4 2003 GCDC time-dependently induced caspase 3 (3.4-fold)- and caspase 9 (1.4-fold)-mediated apoptosis of cholangiocytes, but this was inhibited by lecithins and TUDC. Glycochenodeoxycholic Acid 0-4 caspase 9 Mus musculus 56-65 12857937-2 2003 Here we demonstrate in a mouse macrophage cell line (MH-S cells) that alpha-quartz silica exposure (12.5 mug/cm2 to 50 mug/cm2) elicited activation of both caspase 3 and caspase 9, whereas anatase titanium dioxide (TiO2), a non-fibrogenic particle, did not. Silicon Dioxide 83-89 caspase 9 Mus musculus 170-179 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). Silicon Dioxide 0-6 caspase 9 Mus musculus 65-74 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). Silicon Dioxide 0-6 caspase 9 Mus musculus 185-194 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 160-169 caspase 9 Mus musculus 65-74 12972296-7 2003 In addition, DEX also induced the activation of caspase-9. Dexamethasone 13-16 caspase 9 Mus musculus 48-57 12746256-5 2003 In contrast to p21(+/+) MPTC, cisplatin activated caspase-9 but not caspase-8 in p21(-/-) MPTC before caspase-3 activation. Cisplatin 30-39 caspase 9 Mus musculus 50-59 12746256-9 2003 We conclude that 1) in the presence of p21, cisplatin activates caspase-3 through a mechanism independent of caspase-8 or caspase-9; 2) in the absence of p21, caspase-9 activation precedes caspase-3 activation; 3) the lack of p21 accelerates caspase-3 activation and cisplatin-induced MPTC apoptosis; and 4) MPTC apoptosis is caspase independent in the presence of p21 but partially dependent on caspases in the absence of p21. Cisplatin 44-53 caspase 9 Mus musculus 159-168 12857937-5 2003 Silica-induced apoptosis and caspase 3 activation were, in part, caspase 9 dependent, as determined by their sensitivity to either a general caspase inhibitor (Z-VAD-FMK) or a specific caspase 9 inhibitor (Z-LEHD-FMK). benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 206-216 caspase 9 Mus musculus 185-194 12857937-7 2003 Cyclosporin A, an inhibitor of the mitochondrial permeability pore, partially decreased mitochondrial depolarization, caspase 3 activation, and caspase 9 activation, suggesting a role for mitochondrial dysfunction in these events. Cyclosporine 0-13 caspase 9 Mus musculus 144-153 12857937-8 2003 Pepstatin A, an inhibitor of cathepsin D, also decreased mitochondrial depolarization, caspase 3 activation, and caspase 9 activation, whereas leupeptin, an inhibitor of cathepsin B, had no effect. pepstatin 0-11 caspase 9 Mus musculus 113-122 12857937-9 2003 These data suggest that short-term silica exposure in vitro induces both caspase 3 and caspase 9 activity, which appears to participate in apoptosis. Silicon Dioxide 35-41 caspase 9 Mus musculus 87-96 12738797-5 2003 Serotonin prevents cytochrome c release and caspase-9 and -3 activation after serum deprivation via cross-talks between phosphatidylinositol-3 kinase/Akt and extracellular signal-regulated kinase (ERK) 1/2 signaling pathways. Serotonin 0-9 caspase 9 Mus musculus 44-60 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. Paraoxon 68-71 caspase 9 Mus musculus 31-52 12787408-10 2003 We also observed the presence of active caspase 9 and 3 during apoptosis induced by simvastatin. Simvastatin 84-95 caspase 9 Mus musculus 40-55 12831782-4 2003 Pretreatment of EL4 cells with the caspase-9-specific inhibitor zLEHD-fmk attenuated POX-induced apoptosis in a dose-dependent manner, whereas the caspase-8 inhibitor zIETD-fmk had no effect. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 64-73 caspase 9 Mus musculus 35-44 12831782-4 2003 Pretreatment of EL4 cells with the caspase-9-specific inhibitor zLEHD-fmk attenuated POX-induced apoptosis in a dose-dependent manner, whereas the caspase-8 inhibitor zIETD-fmk had no effect. Paraoxon 85-88 caspase 9 Mus musculus 35-44 12832530-5 2003 Immunoblot and biochemical analysis also confirmed that activation of both caspase-9 and caspase-3 was induced by 6-OHDA, but not by MPP+. Oxidopamine 114-120 caspase 9 Mus musculus 75-84 12832530-5 2003 Immunoblot and biochemical analysis also confirmed that activation of both caspase-9 and caspase-3 was induced by 6-OHDA, but not by MPP+. mangion-purified polysaccharide (Candida albicans) 133-137 caspase 9 Mus musculus 75-84 12832530-8 2003 Interestingly, a reconstitution assay indicated that the addition of ATP to the cytosolic fraction obtained from MPP+-treated cells was sufficient to activate both caspase-9 and caspase-3. Adenosine Triphosphate 69-72 caspase 9 Mus musculus 164-173 12832530-8 2003 Interestingly, a reconstitution assay indicated that the addition of ATP to the cytosolic fraction obtained from MPP+-treated cells was sufficient to activate both caspase-9 and caspase-3. mangion-purified polysaccharide (Candida albicans) 113-117 caspase 9 Mus musculus 164-173 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. Paraoxon 68-71 caspase 9 Mus musculus 168-177 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 126-135 caspase 9 Mus musculus 31-52 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 126-135 caspase 9 Mus musculus 168-177 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. Paraoxon 214-217 caspase 9 Mus musculus 31-52 12831782-5 2003 Furthermore, the activation of caspase-9, -8, and -3 in response to POX treatment was completely inhibited in the presence of zLEHD-fmk, implicating the involvement of caspase 9-dependent mitochondrial pathways in POX-stimulated apoptosis. Paraoxon 214-217 caspase 9 Mus musculus 168-177 12831782-11 2003 The results indicate that POX induces apoptosis in EL4 cells through a direct effect on mitochondria by disrupting its transmembrane potential, causing the release of cytochrome c into the cytosol and subsequent activation of caspase-9. Paraoxon 26-29 caspase 9 Mus musculus 226-235 12857599-8 2003 Securioside B plus L-cell-conditioned medium induced the activation of caspase-3 and caspase-9, but not caspase-8. securioside B 0-13 caspase 9 Mus musculus 85-94 12685655-8 2003 These results showed that the inhibition of the caspase cascade downstream mitochondria by ROS production, leading to a significant inhibition of caspase-3/7 activation, was one of the causes of the antiapoptotic effect by small doses of UVB irradiation. Reactive Oxygen Species 91-94 caspase 9 Mus musculus 48-55 12505448-4 2003 The initiator caspases (caspase-8 and caspase-9) as well as the effector caspase (caspase-3) were activated by the treatment of L929 cells with malathion. Malathion 144-153 caspase 9 Mus musculus 38-47 12581736-7 2003 The dominant negative form of FADD and z-VAD-fmk inhibited caspase-8, caspase-9, Bid processing, cytochrome c release, and DNA fragmentation induced by ER stress, suggesting that caspase-8 and caspase-9 are the main caspases involved in ER stress-mediated apoptosis of P19-36/12 (-) cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 39-48 caspase 9 Mus musculus 70-79 12581736-7 2003 The dominant negative form of FADD and z-VAD-fmk inhibited caspase-8, caspase-9, Bid processing, cytochrome c release, and DNA fragmentation induced by ER stress, suggesting that caspase-8 and caspase-9 are the main caspases involved in ER stress-mediated apoptosis of P19-36/12 (-) cells. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 39-48 caspase 9 Mus musculus 193-202 12660414-5 2003 Administration of a caspase-9 inhibitor (Ac-IETD-CHO) effectively prevented both ureteric bud branching and nephrogenesis, the same as a caspase-3 inhibitor (Ac-DEVD-CHO). Ac-IETD-CHO 41-52 caspase 9 Mus musculus 20-29 12662968-4 2003 Mitochondrial involvement is evident due to the loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol and activation of caspase-9 in dexamethasone-treated thymocytes. Dexamethasone 167-180 caspase 9 Mus musculus 154-163 12662968-5 2003 The addition of spermine inhibited the release of cytochrome c from the mitochondria into the cytosol, and also the activation of caspase-9. Spermine 16-24 caspase 9 Mus musculus 130-139 12538035-6 2003 Part of CMT-induced PCD is due to the activation of caspase-9, since it is reduced by the specific caspase-9 inhibitor, Z-LEHD-fmk. cmt 8-11 caspase 9 Mus musculus 52-61 12538035-6 2003 Part of CMT-induced PCD is due to the activation of caspase-9, since it is reduced by the specific caspase-9 inhibitor, Z-LEHD-fmk. cmt 8-11 caspase 9 Mus musculus 99-108 12538035-6 2003 Part of CMT-induced PCD is due to the activation of caspase-9, since it is reduced by the specific caspase-9 inhibitor, Z-LEHD-fmk. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 120-130 caspase 9 Mus musculus 52-61 12538035-6 2003 Part of CMT-induced PCD is due to the activation of caspase-9, since it is reduced by the specific caspase-9 inhibitor, Z-LEHD-fmk. benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone 120-130 caspase 9 Mus musculus 99-108 22692436-8 2002 Studies were conducted using the highly malignant +SA mouse mammary epithelial cell line to determine if tocotrienol-induced programmed cell death is mediated through the caspase-8 or caspase-9 pathway. Tocotrienols 105-116 caspase 9 Mus musculus 184-193 12881019-4 2003 Studies were conducted to determine whether tocotrienol-induced apoptosis is mediated by activation of the caspase-8 and/or caspase-9 pathway. Tocotrienols 44-55 caspase 9 Mus musculus 124-133 12881019-8 2003 Additional studies showed that treatment with 50 mM TRF or 20 mM g-tocotrienol increased intracellular activity and levels of processed caspase-8 and -3 but not caspase-9. g-tocotrienol 65-78 caspase 9 Mus musculus 161-170 12881019-10 2003 These findings demonstrate that tocotrienol-induced apoptosis in +SA mammary cancer cells is mediated through activation of the caspase-8 signaling pathway and is independent of caspase-9 activation. Tocotrienols 32-43 caspase 9 Mus musculus 178-187 12351727-5 2002 Our data indicate that both upstream caspase-8 and upstream caspase-9, as well as downstream caspase-3 are activated in hair cells exposed to neomycin. Neomycin 142-150 caspase 9 Mus musculus 60-69 12351727-6 2002 The inhibition of caspase-9-like activity provided significant protection of hair cells exposed to neomycin, whereas the inhibition of caspase-8-like activity was not effective in preventing neomycin-induced hair cell death. Neomycin 99-107 caspase 9 Mus musculus 18-27 12351727-8 2002 These data indicate that caspase-9 is the primary upstream caspase mediating neomycin-induced hair cell death in this preparation. Neomycin 77-85 caspase 9 Mus musculus 25-34 12027451-0 2002 The p53 stabilizing compound CP-31398 induces apoptosis by activating the intrinsic Bax/mitochondrial/caspase-9 pathway. CP 31398 29-37 caspase 9 Mus musculus 102-111 12027451-7 2002 Taken together, our results indicate that CP-31398 induces p53-dependent apoptosis by activating the Bax/mitochondrial/caspase-9 pathway. CP 31398 42-50 caspase 9 Mus musculus 119-128 12051998-2 2002 Herein we show that hyperthermia, 4-hydroperoxycyclophosphamide, and staurosporine also activate caspase-9, the apical caspase in the mitochondrial apoptotic pathway. perfosfamide 34-63 caspase 9 Mus musculus 97-106 12051998-2 2002 Herein we show that hyperthermia, 4-hydroperoxycyclophosphamide, and staurosporine also activate caspase-9, the apical caspase in the mitochondrial apoptotic pathway. Staurosporine 69-82 caspase 9 Mus musculus 97-106 11861645-3 2002 Nitric oxide administered during hypoxia induced the release of cytochrome c, caspase-9 activation, and the loss of mitochondrial membrane potential followed by DNA fragmentation and lactate dehydrogenase release (markers of cell death). Nitric Oxide 0-12 caspase 9 Mus musculus 78-87 11861645-4 2002 Bcl-X(L) protected cells from nitric oxide-induced apoptosis during hypoxia by preventing the release of cytochrome c, caspase-9 activation, and by maintaining a mitochondrial membrane potential. Nitric Oxide 30-42 caspase 9 Mus musculus 119-128 11967922-15 2002 Work from my laboratory in the last 5 years has shown that teratogens, such as hyperthermia, 4-hydroperoxycyclophosphamide, and staurosporine, induce cell death in day 9 mouse embryos by activating the mitochondrial apoptotic pathway, i.e., mitochondrial release of cytochrome c, activation of caspase-9 and -3, inactivation of poly (ADP-ribose) polymerase (PARP), and systematic degradation of DNA. perfosfamide 93-122 caspase 9 Mus musculus 294-310 11967922-15 2002 Work from my laboratory in the last 5 years has shown that teratogens, such as hyperthermia, 4-hydroperoxycyclophosphamide, and staurosporine, induce cell death in day 9 mouse embryos by activating the mitochondrial apoptotic pathway, i.e., mitochondrial release of cytochrome c, activation of caspase-9 and -3, inactivation of poly (ADP-ribose) polymerase (PARP), and systematic degradation of DNA. Staurosporine 128-141 caspase 9 Mus musculus 294-310 11953831-3 2002 The broad spectrum caspase inhibitor zVADfmk and caspase-9 inhibitor zLEDHfmk inhibited apoptosis and improved cell viability when administrated to cells 1 h before exposure to declopramide, whereas the caspase-8 inhibitor zIEDHfmk had less effect. zledhfmk 69-77 caspase 9 Mus musculus 49-58 11953831-3 2002 The broad spectrum caspase inhibitor zVADfmk and caspase-9 inhibitor zLEDHfmk inhibited apoptosis and improved cell viability when administrated to cells 1 h before exposure to declopramide, whereas the caspase-8 inhibitor zIEDHfmk had less effect. declopramide 177-189 caspase 9 Mus musculus 49-58 11953831-3 2002 The broad spectrum caspase inhibitor zVADfmk and caspase-9 inhibitor zLEDHfmk inhibited apoptosis and improved cell viability when administrated to cells 1 h before exposure to declopramide, whereas the caspase-8 inhibitor zIEDHfmk had less effect. ziedhfmk 223-231 caspase 9 Mus musculus 49-58 11331615-0 2001 Altered proteasomal function due to the expression of polyglutamine-expanded truncated N-terminal huntingtin induces apoptosis by caspase activation through mitochondrial cytochrome c release. polyglutamine 54-67 caspase 9 Mus musculus 130-137 11739725-3 2002 The death observed during oxygen deprivation involves a decrease in the mitochondrial membrane potential, followed by the release of cytochrome c and the activation of caspase-9. Oxygen 26-32 caspase 9 Mus musculus 168-177 11739725-4 2002 Bcl-X(L) prevented oxygen deprivation-induced cell death by inhibiting the release of cytochrome c and caspase-9 activation. Oxygen 19-25 caspase 9 Mus musculus 103-112 11739563-0 2001 Caspase-9 activation results in downstream caspase-8 activation and bid cleavage in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 84-128 caspase 9 Mus musculus 0-9 11739563-5 2001 MPTP was found to elicit not only the activation of the effector caspase-3 but also the initiators caspase-8 and caspase-9, mitochondrial cytochrome c release, and Bid cleavage in the SN of wild-type mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 caspase 9 Mus musculus 113-122 11739563-8 2001 MPTP-associated toxicity in culture was found temporally to involve cytochrome c release, activation of caspase-9, caspase-3, and caspase-8, and Bid cleavage. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 0-4 caspase 9 Mus musculus 104-113 11739563-10 2001 Activated caspase-8 and caspase-9 were immunologically detectable within MPP(+)-treated mesencephalic dopaminergic neurons, dopaminergic nigral neurons from MPTP-treated mice, and autopsied Parkinsonian tissue from late-onset sporadic cases of the disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 157-161 caspase 9 Mus musculus 24-33 11739563-11 2001 These data demonstrate that MPTP-mediated activation of caspase-9 via cytochrome c release results in the activation of caspase-8 and Bid cleavage, which we speculate may be involved in the amplification of caspase-mediated dopaminergic cell death. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 28-32 caspase 9 Mus musculus 56-65 11533046-11 2001 Thus, FC loading, perhaps via increased levels of Bax and/or cholesterol overloading of mitochondria, triggers cytochrome c release and activation of caspase-9 and the effector caspases, leading to macrophage apoptosis. Fc(alpha) receptor 6-8 caspase 9 Mus musculus 150-159 11485400-8 2001 The caspase-3-like protease specific inhibitor, Ac-DEVD-CHO peptide, partially inhibited E protein- or caspase-9-induced apoptosis in Neuro-2a cells. acetyl-aspartyl-glutamyl-valyl-aspartal 48-59 caspase 9 Mus musculus 103-112 11333366-7 2001 Cleaved caspase-9 first appeared in the cytosol at 2 hours and colocalized with cytochrome c. Terminal deoxynucleotidyl transferase-mediated uridine 5;-triphosphate-biotin nick and labeling (TUNEL) showed significant increase of positive cells in Sod2 -/+ mice compared with the wild-type in the cortex, but not in the caudate putamen. triphosphoric acid 152-164 caspase 9 Mus musculus 8-17 11333366-7 2001 Cleaved caspase-9 first appeared in the cytosol at 2 hours and colocalized with cytochrome c. Terminal deoxynucleotidyl transferase-mediated uridine 5;-triphosphate-biotin nick and labeling (TUNEL) showed significant increase of positive cells in Sod2 -/+ mice compared with the wild-type in the cortex, but not in the caudate putamen. Biotin 165-171 caspase 9 Mus musculus 8-17 11256964-0 2001 Effect of polyamine depletion on caspase activation: a study with spermine synthase-deficient cells. Polyamines 10-19 caspase 9 Mus musculus 33-40 11256964-2 2001 The requirement for spermine for the processes leading to caspase activation has been studied in transformed embryonic fibroblasts obtained from gyro (Gy) mutant male mice. Spermine 20-28 caspase 9 Mus musculus 58-65 11256964-6 2001 The lack of spermine did not affect the expression of Bcl-2, and caspases 3 and 9 were activated by etoposide in both N and Gy cells, indicating that spermine is dispensable for caspase activation. Etoposide 100-109 caspase 9 Mus musculus 65-72 11256964-7 2001 Spermine deficiency did not significantly influence caspase activity in cells treated with etoposide, cycloheximide or staurosporine, but sensitized the cells to UV irradiation, which triggered significantly higher caspase activity in Gy cells compared with N cells. Spermine 0-8 caspase 9 Mus musculus 215-222 11256964-9 2001 This depletion, which included spermine deficiency, dramatically increased caspase activation and cell death in Gy fibroblasts exposed to UV irradiation. Spermine 31-39 caspase 9 Mus musculus 75-82 11256964-11 2001 In Gy cells depleted of polyamines by DFMO, polyamine replenishment with either spermidine or spermine was sufficient to restore caspase activity induced by etoposide, indicating that, in this model, polyamines have an interchangeable role in supporting caspase activation. Spermidine 80-90 caspase 9 Mus musculus 129-136 11256964-11 2001 In Gy cells depleted of polyamines by DFMO, polyamine replenishment with either spermidine or spermine was sufficient to restore caspase activity induced by etoposide, indicating that, in this model, polyamines have an interchangeable role in supporting caspase activation. Spermine 94-102 caspase 9 Mus musculus 129-136 11256964-11 2001 In Gy cells depleted of polyamines by DFMO, polyamine replenishment with either spermidine or spermine was sufficient to restore caspase activity induced by etoposide, indicating that, in this model, polyamines have an interchangeable role in supporting caspase activation. Etoposide 157-166 caspase 9 Mus musculus 129-136 11256964-11 2001 In Gy cells depleted of polyamines by DFMO, polyamine replenishment with either spermidine or spermine was sufficient to restore caspase activity induced by etoposide, indicating that, in this model, polyamines have an interchangeable role in supporting caspase activation. Polyamines 200-210 caspase 9 Mus musculus 254-261 11256964-12 2001 Therefore, spermine is not required for such activation, and the effect and specificity of polyamine depletion on caspase activity may be very different, depending on the role of polyamines in the specific death pathways engaged by different stimuli. Polyamines 91-100 caspase 9 Mus musculus 114-121 11256964-12 2001 Therefore, spermine is not required for such activation, and the effect and specificity of polyamine depletion on caspase activity may be very different, depending on the role of polyamines in the specific death pathways engaged by different stimuli. Polyamines 179-189 caspase 9 Mus musculus 114-121 11256964-13 2001 Some inducers of apoptosis, for example etoposide, absolutely require polyamines for caspase activation, yet the lack of polyamines, particularly spermine, strongly increases caspase activation when induced by UV irradiation. Etoposide 40-49 caspase 9 Mus musculus 85-92 11256964-13 2001 Some inducers of apoptosis, for example etoposide, absolutely require polyamines for caspase activation, yet the lack of polyamines, particularly spermine, strongly increases caspase activation when induced by UV irradiation. Polyamines 70-80 caspase 9 Mus musculus 85-92 11256964-13 2001 Some inducers of apoptosis, for example etoposide, absolutely require polyamines for caspase activation, yet the lack of polyamines, particularly spermine, strongly increases caspase activation when induced by UV irradiation. Polyamines 121-131 caspase 9 Mus musculus 175-182 11256964-13 2001 Some inducers of apoptosis, for example etoposide, absolutely require polyamines for caspase activation, yet the lack of polyamines, particularly spermine, strongly increases caspase activation when induced by UV irradiation. Spermine 146-154 caspase 9 Mus musculus 175-182 11550085-3 2001 Using these antisera and caspase-9- and caspase-3-deficient mouse embryonic fibroblasts, we demonstrated that mouse caspase-9 is initially autoprocessed at D(353) and D(368) at low levels during staurosporine-induced apoptosis, whereupon the D(368) and D(168) sites are preferentially processed over D(353) by activated caspase-3 as part of a feedback amplification loop. Staurosporine 195-208 caspase 9 Mus musculus 116-125 11550085-4 2001 Ac-DEVD-MCA (caspase-3-like) and Ac-LEHD-MCA (caspase-9-like) cleavage activities clearly showed that caspase-9 autoprocessing was necessary for the activation of caspase-3, whereas full activation of caspase-3 and caspase-9 was achieved only through the feedback amplification loop. DEVD 3-7 caspase 9 Mus musculus 102-111 11550085-4 2001 Ac-DEVD-MCA (caspase-3-like) and Ac-LEHD-MCA (caspase-9-like) cleavage activities clearly showed that caspase-9 autoprocessing was necessary for the activation of caspase-3, whereas full activation of caspase-3 and caspase-9 was achieved only through the feedback amplification loop. DEVD 3-7 caspase 9 Mus musculus 102-111 11182320-4 2001 Cell killing induced by apoptolidin was independent of p53 status, inhibited by BCL-2, and dependent on the action of caspase-9. apoptolidin 24-35 caspase 9 Mus musculus 118-127 11367518-0 2001 Involvement of mitochondrial permeability transition and caspase-9 activation in dimethyl sulfoxide-induced apoptosis of EL-4 lymphoma cells. Dimethyl Sulfoxide 81-99 caspase 9 Mus musculus 57-66 11367518-5 2001 In the involvement of caspases, caspase-9 and -3, but not caspase-8, were found to be activated responding to DMSO treatment. Dimethyl Sulfoxide 110-114 caspase 9 Mus musculus 32-48 11062535-3 2000 Using an established in vivo model of Fas-mediated apoptosis, we demonstrate here that elimination of certain caspases was compensated in vivo by the activation of other caspases. ammonium ferrous sulfate 38-41 caspase 9 Mus musculus 110-118 11062535-3 2000 Using an established in vivo model of Fas-mediated apoptosis, we demonstrate here that elimination of certain caspases was compensated in vivo by the activation of other caspases. ammonium ferrous sulfate 38-41 caspase 9 Mus musculus 170-178 10807576-5 2000 When ectopically expressed, Noxa underwent BH3 motif-dependent localization to mitochondria and interacted with anti-apoptotic Bcl-2 family members, resulting in the activation of caspase-9. BH 3 43-46 caspase 9 Mus musculus 180-189 10660524-4 2000 Moreover, phosphatidylinositol 4, 5-bisphosphate-gelsolin strongly inhibits caspase-3 and -9 activity through the formation of a stable phosphatidylinositol 4, 5-bisphosphate-gelsolin-caspase complex. Phosphatidylinositol 4,5-Diphosphate 10-48 caspase 9 Mus musculus 76-83 10660524-4 2000 Moreover, phosphatidylinositol 4, 5-bisphosphate-gelsolin strongly inhibits caspase-3 and -9 activity through the formation of a stable phosphatidylinositol 4, 5-bisphosphate-gelsolin-caspase complex. Phosphatidylinositol 4,5-Diphosphate 136-174 caspase 9 Mus musculus 76-83 10660524-5 2000 In addition, phosphatidylinositol 4,5-bisphosphate-gelsolin prevents apoptotic progression mediated by caspase-3 in a cell-free system, and phosphatidylinositol 4,5-bisphosphate-gelsolin-caspase-9 and phosphatidylinositol 4,5-bisphosphate-gelsolin-caspase-3 complexes form in mouse embryonic fibroblasts during apoptosis induction when stimulated with fibronectin, to delay cell death. Phosphatidylinositol 4,5-Diphosphate 140-177 caspase 9 Mus musculus 187-196 10660524-5 2000 In addition, phosphatidylinositol 4,5-bisphosphate-gelsolin prevents apoptotic progression mediated by caspase-3 in a cell-free system, and phosphatidylinositol 4,5-bisphosphate-gelsolin-caspase-9 and phosphatidylinositol 4,5-bisphosphate-gelsolin-caspase-3 complexes form in mouse embryonic fibroblasts during apoptosis induction when stimulated with fibronectin, to delay cell death. Phosphatidylinositol 4,5-Diphosphate 140-177 caspase 9 Mus musculus 187-196 25887954-9 2015 PKA inhibitor abolished the effects of DOB on caspase-9 activation, Bcl-2 levels as well as JNK and p38 MAPK phosphorylation, but not on IkappaBalpha phosphorylation, TNF-alpha expression and caspase-8 activation in LPS-stimulated cardiomyocytes. Dobutamine 39-42 caspase 9 Mus musculus 46-55 33782744-8 2021 TUNEL staining and the protein expression levels of cleaved caspase-3 and cleaved caspase-9 were used to detect cell apoptosis and results make clear that DEX can reduce the apoptosis caused by myocardial infarction. Dexmedetomidine 155-158 caspase 9 Mus musculus 82-91 25887954-10 2015 Pretreatment with nifedipine not only significantly blocked the enhancing effects of DOB on LPS-induced elevation in cytosolic Ca(2+) concentration and CaMKII phosphorylation in cardiomyocytes, but also partly reversed the effects of DOB on caspase-9 and caspase-3/7 activities in LPS-treated cardiomyocytes. Nifedipine 18-28 caspase 9 Mus musculus 241-250 25887954-10 2015 Pretreatment with nifedipine not only significantly blocked the enhancing effects of DOB on LPS-induced elevation in cytosolic Ca(2+) concentration and CaMKII phosphorylation in cardiomyocytes, but also partly reversed the effects of DOB on caspase-9 and caspase-3/7 activities in LPS-treated cardiomyocytes. Dobutamine 85-88 caspase 9 Mus musculus 241-250 34737012-18 2022 PB pretreatment also downregulated the apoptotic factors caspase-3, caspase-9, and apoptotic protein Bax, and it upregulated apoptotic protein Bcl-2. physalin B 0-2 caspase 9 Mus musculus 68-77 34811512-4 2022 Furthermore, Rb1 treatment reversed high glucose-induced increases in Cyto c, Caspase 9 and mitochondrial regulatory protein NOX4, but did not affect the upregulated expression of aldose reductase (AR). Glucose 41-48 caspase 9 Mus musculus 78-87 34517333-5 2022 The results showed that fluoride reduced the bodyweight and liver coefficient, increased the bone fluoride content, the aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamate dehydrogenase (GDH) levels, caspase 8 and caspase 9 activities, and induced liver morphology and ultrastructure damage. Fluorides 24-32 caspase 9 Mus musculus 238-247 34351278-7 2022 Results revealed that the mRNA contents of APAF-1, CYTC, and CASP-9 related genes were significantly decreased after butachlor treatment. butachlor 117-126 caspase 9 Mus musculus 61-67 34911926-6 2021 The expression of apoptosis-related caspase-3 and caspase-9 was detected by western blot analysis The tumor growth in the mouse xenograft model of NPC treated with thiostrepton or control was assessed. Thiostrepton 164-176 caspase 9 Mus musculus 50-59 34374636-5 2021 At a concentration-dependent way, resveratrol reversed H2O2-induced increases in expressions of cleaved caspase-3 and cleaved caspase-9, production of ROS, loss of mitochondrial membrane potential and the expressions of p-p38, p-ERK, and p-JNK. Resveratrol 34-45 caspase 9 Mus musculus 126-135 34374636-5 2021 At a concentration-dependent way, resveratrol reversed H2O2-induced increases in expressions of cleaved caspase-3 and cleaved caspase-9, production of ROS, loss of mitochondrial membrane potential and the expressions of p-p38, p-ERK, and p-JNK. Hydrogen Peroxide 55-59 caspase 9 Mus musculus 126-135 34910443-7 2021 Under the intervention of high glucose, ERK/JAK-STAT/NF-kappaB inhibitors brilliantly diminished the up-regulation of caspase-9 (p < 0.05), and ERK/JAK-STAT inhibitors notably minimized the up-regulation of NF-kappaB p65 (p < 0.05). Glucose 31-38 caspase 9 Mus musculus 118-127 34264144-13 2021 LOX-1 neutralizing antibody or Poly I treatment significantly decreased neutrophil infiltration, the quantity of TUNEL-positive cells, the expression of Fas, Fas ligand, caspase-8, caspase-9, caspase-3, BCL2, cleaved caspase-3 and the percentage of apoptosis neutrophils compared with control corneas. poly i 31-37 caspase 9 Mus musculus 181-190 34525396-5 2021 Treatment with MitoQ also suppressed LPS/D-Gal-induced production of tumor necrosis factor alpha (TNF-alpha), inhibited the activities of caspase-3, caspase-8 and caspase-9, decreased the level of cleaved caspase-3 and reduced the counts of TUNEL positive cells. mitoquinone 15-20 caspase 9 Mus musculus 163-172 34400214-7 2021 Furthermore, increased levels of cleaved caspase 3, cleaved caspase 7, cleaved caspase 9, cleaved poly (ADP-ribose) polymerase (PARP) and Bax and reduced levels of Bcl2 in LPS-treated mice and HK-2 cells were reversed after Ala administration. alamandine 224-227 caspase 9 Mus musculus 79-88 34846706-7 2022 Furthermore, astragalin dramatically rescued the gene expression related to spermatogenesis (AKT1, BCL-2, CASPASE9, CASPASE3, MAPKAPK2, RPS6KA5, STAR, and PRKACB), and increased the level of testosterone by improving related proteins (STAR, CYP11A1, PRKACB) for oligoasthenozoospermia induced by CTX. astragalin 13-23 caspase 9 Mus musculus 106-114 34699866-6 2021 Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2. ponatinib 21-30 caspase 9 Mus musculus 108-117 34699866-6 2021 Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2. Gossypol 31-39 caspase 9 Mus musculus 108-117 34174222-9 2021 RESULTS: The results showed that acteoside inhibited melanoma growth, alleviated inflammation levels in mice, attenuated ROS and apoptosis levels in the spleen, downregulated the levels of CD31, survivin, Ras, Raf1, p-STAT3, and Bcl-2, and upregulated the levels of ERbeta, Bax, cleaved caspase-3, and cleaved caspase-9. acteoside 33-42 caspase 9 Mus musculus 310-319 34956620-8 2021 In HK-2 cells, fructose promoted the secretion of TNF-alpha, IL-1beta and IL-6 and increased the levels of RAGE, p-IkappaBalpha, p-NF-kappaB, bax, caspase-3 and caspase-9, but decreased the levels of Bcl-2. Fructose 15-23 caspase 9 Mus musculus 161-170 34899328-14 2021 Geniposide increased the protein expression of B-cell lymphoma-2 (Bcl-2) and downregulated the protein expression of Bcl-2 Associated X (Bax), cleaved-Caspase 3, and cleaved-Caspase 9. geniposide 0-10 caspase 9 Mus musculus 174-183 34669944-12 2021 Consistent with increasing expressions of Bax, cleaved-caspase-9/-3, and a decrease of Bcl-2 level, typical apoptotic ultrastructure, and apoptosis-positive cells were also observed in the selenium-deficient placenta of mice. Selenium 189-197 caspase 9 Mus musculus 55-64 34146870-7 2021 The results on the mechanisms of liver toxicity indicated that butachlor induced overexpression of Apaf-1, Bax, Caspase-3, Caspase-9, Cyt-c, p53, Beclin-1, ATG-5, and LC3, whereas decreases the expression of Bcl-2 and p62 suggesting abnormal processes of apoptosis and autophagy. butachlor 63-72 caspase 9 Mus musculus 123-132 34569560-7 2021 Intriguingly, TPs treatment increased the expression of Bak1, cleaved caspase-9 and cleaved caspase-3, but decreased the level of Bcl-2 and mitochondrial membrane potential, which indicated that TPs induced mitochondrial-mediated apoptosis. tissue polypeptide specific antigen 14-17 caspase 9 Mus musculus 70-79 34569560-7 2021 Intriguingly, TPs treatment increased the expression of Bak1, cleaved caspase-9 and cleaved caspase-3, but decreased the level of Bcl-2 and mitochondrial membrane potential, which indicated that TPs induced mitochondrial-mediated apoptosis. tissue polypeptide specific antigen 195-198 caspase 9 Mus musculus 70-79 34439516-9 2021 Moreover, LUTN treatment considerably attenuates the AFB1-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Luteolin 10-14 caspase 9 Mus musculus 184-193 34630081-9 2021 Also, GA protected against ANIT-induced mitochondrial apoptosis by regulating the expression of Bcl-2, Bax, cleaved caspase 3 and cleaved caspase 9. Glycyrrhetinic Acid 6-8 caspase 9 Mus musculus 138-147 34303733-4 2021 GC-2 cells were treated with PFOS (0, 50, 100 and 150microM) for 24 h or 48 h. Results demonstrated that PFOS dose-dependently inhibited cell viability, induced G0/G1 cell cycle arrest and triggered apoptosis, which might be partly explained by the decrease in cyclin D1, PCNA and Bcl-2 protein expression; increase in Bax protein expression; and activation of caspase-9, -3. perfluorooctane sulfonic acid 29-33 caspase 9 Mus musculus 361-370 34223821-12 2021 Caspase-8 and caspase-9 inhibitors protected pancreatic beta-cells from dexamethasone-induced apoptosis. Dexamethasone 72-85 caspase 9 Mus musculus 14-23 34165156-12 2021 The results indicated that LRC regulated dexamethasone-induced osteoblast apoptotic markers, including caspase-6, caspase-9, X-linked inhibitor of apoptosis, apoptosis inhibitor 1 and apoptosis inhibitor 2, and increased the expression of osteoblast differentiation-related genes, such as Runt-related transcription factor 2 and bone morphogenetic protein 2 in the MC3T3E-1 cell line. Dexamethasone 41-54 caspase 9 Mus musculus 114-123 34303733-4 2021 GC-2 cells were treated with PFOS (0, 50, 100 and 150microM) for 24 h or 48 h. Results demonstrated that PFOS dose-dependently inhibited cell viability, induced G0/G1 cell cycle arrest and triggered apoptosis, which might be partly explained by the decrease in cyclin D1, PCNA and Bcl-2 protein expression; increase in Bax protein expression; and activation of caspase-9, -3. perfluorooctane sulfonic acid 105-109 caspase 9 Mus musculus 361-370 34393792-10 2021 8-Gin also could lead to down-regulation of the activities of matrix metalloproteinases-9 (MMP-9), Caspase-9, and Bax protein, up-regulation of the activity of Bcl-2 protein, and alleviation of cardiomyocyte apoptosis. 8-gingerol 0-5 caspase 9 Mus musculus 99-108 35413363-6 2022 Meanwhile, co-treatment with As and PSNPs induced apoptosis in the liver, which was confirmed by ultrastructure observation and changes in the expression of apoptosis indicators (P53, Bax, Bcl-2, Caspase-3, Caspase-9, Cleaved-Caspase-3 and Cytc). Arsenic 29-31 caspase 9 Mus musculus 207-216 34299239-6 2021 Results from this study revealed that the presence of estrogen receptor beta in mitochondria render N2A cells more resistant to staurosporine- and H2O2-induced apoptotic stimuli, as indicated by the reduced activation of caspase-9 and -3, the increased cell viability, the increased ATP production, and the increased resistance to mitochondrial impairment in the presence or absence of 17-beta estradiol (E2). Staurosporine 128-141 caspase 9 Mus musculus 221-237 34299239-6 2021 Results from this study revealed that the presence of estrogen receptor beta in mitochondria render N2A cells more resistant to staurosporine- and H2O2-induced apoptotic stimuli, as indicated by the reduced activation of caspase-9 and -3, the increased cell viability, the increased ATP production, and the increased resistance to mitochondrial impairment in the presence or absence of 17-beta estradiol (E2). Hydrogen Peroxide 147-151 caspase 9 Mus musculus 221-237 34299239-6 2021 Results from this study revealed that the presence of estrogen receptor beta in mitochondria render N2A cells more resistant to staurosporine- and H2O2-induced apoptotic stimuli, as indicated by the reduced activation of caspase-9 and -3, the increased cell viability, the increased ATP production, and the increased resistance to mitochondrial impairment in the presence or absence of 17-beta estradiol (E2). Estradiol 386-403 caspase 9 Mus musculus 221-237 35623085-7 2022 In vitro, we found duloxetine notably inhibits the relative mRNA and protein expression levels of p53, Bax/Bcl2, caspase-3, and caspase-9 in DRG neurons, which may indicate duloxetine protected the DRG neuron by inhibiting p53-related pathways. Duloxetine Hydrochloride 19-29 caspase 9 Mus musculus 128-137 35623085-7 2022 In vitro, we found duloxetine notably inhibits the relative mRNA and protein expression levels of p53, Bax/Bcl2, caspase-3, and caspase-9 in DRG neurons, which may indicate duloxetine protected the DRG neuron by inhibiting p53-related pathways. Duloxetine Hydrochloride 173-183 caspase 9 Mus musculus 128-137 35485954-6 2022 We discovered that LS-HB located in the mitochondria of B16F10 cells was able to generate excess reactive oxygen species, which subsequently resulted in mitochondrial membrane potential loss and induced apoptosis via caspase-9 and caspase-3 pathways. Reactive Oxygen Species 97-120 caspase 9 Mus musculus 217-226 35617905-10 2022 Immunohistochemistry and RT-qPCR showed that the expression of Bax, caspase-3 and caspase-9 significantly increased in the MCZ- group. mancozeb 123-126 caspase 9 Mus musculus 82-91 35585377-4 2022 The numbers of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Hydrogen Peroxide 95-99 caspase 9 Mus musculus 74-83 35529482-10 2022 Dex inhibited MC3T3-E1 cell viability in a dose-dependent effect and induced apoptosis by increasing the expression levels of FOXO1, Bax, cleaved-Caspase-3, and cleaved-Caspase-9, while reducing the expression of Bcl-2. Dexamethasone 0-3 caspase 9 Mus musculus 169-178 35384580-7 2022 The STZ-mediated stimulation of TRPM2 increased the cytosolic Ca2+, lipid peroxidation, mitROS, cytosolic ROS, apoptosis, caspase-3, caspase-8, and caspase-9 concentrations in the mice, although their concentrations were decreased in the optic nerve by the treatments of Se and RSV. Streptozocin 4-7 caspase 9 Mus musculus 148-157 35384580-9 2022 The STZ-induced increase of TRPM2, PARP-1, caspase-3, and caspase-9 protein band expressions was diminished by the treatments of Se and RSV. Streptozocin 4-7 caspase 9 Mus musculus 58-67 35384580-9 2022 The STZ-induced increase of TRPM2, PARP-1, caspase-3, and caspase-9 protein band expressions was diminished by the treatments of Se and RSV. Resveratrol 136-139 caspase 9 Mus musculus 58-67 35471621-7 2022 Moreover, CFE blocked H2O2-induced cytosolic release of cytochrome c, activation of caspase-9 and caspase-3, and degradation of poly (ADP-ribose) polymerase. Hydrogen Peroxide 22-26 caspase 9 Mus musculus 84-93 35278602-6 2022 The in vivo data demonstrated that mice given urethane alone had a significant increase in MDA, NO, NF-kappaB level, HIF1-alpha, and COX-2-positive expression in the lung tissue and serum VEGFR2, ALT, AST, urea, and creatinine accompanied with a significant decrease in GSH, SOD, caspase 9 in the lung tissue and serum BAX. Urethane 46-54 caspase 9 Mus musculus 280-289 35453686-7 2022 hDT806 decreased EGFR protein levels and disrupted the EGFR signaling downstream effectors, including MAPK/ERK1/2 and AKT, while increased proapoptotic proteins, such as p53, caspase-9, caspase-3, and the cleaved PAPR. hdt806 0-6 caspase 9 Mus musculus 175-184 35278602-7 2022 Co-treatment with BBR-COSNPs suppressed lung cancer growth and promoted apoptosis by modulating serum BAX and lung caspase 9 gene expressions. bbr 18-21 caspase 9 Mus musculus 115-124 35344814-5 2022 Additionally, metformin induced cytochrome c release from mitochondria into the cytoplasm, directly triggering caspase-9-mediated mitochondrial apoptosis. Metformin 14-23 caspase 9 Mus musculus 111-120 35019826-12 2022 In addition, mitochondrial membrane depolarization, ROS, caspase-3, caspase-9, and apoptosis values induced by MPP decreased with resveratrol treatment. 1-Methyl-4-phenylpyridinium 111-114 caspase 9 Mus musculus 68-77 35167638-6 2022 Pb(Ac)2 exposure significantly increased cellular oxidative damage and the levels of pro-inflammatory cytokines (interleukin (IL)-1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha), ionized calcium binding adaptor molecule 1 (Iba1) and pro-apoptotic proteins (caspase 3, caspase 9 and Bax), while downregulating the expression of Bcl-2 in the brain. pb(ac)2 0-7 caspase 9 Mus musculus 276-285 35187930-10 2022 Furthermore, TW-7 inhibited the mitochondrial apoptosis pathway by downregulation of the cytoplasmic cytochrome C, caspase-9, and cleaved-caspase-3 expression. tw-7 13-17 caspase 9 Mus musculus 115-124 35236377-10 2022 KO, and KO plus 1/2 dose of oxaliplatin significantly increased the expression of cytochrome c, cleaved caspase-9 and -3, and DNA damage and decreased expression of PD-L1, PD-L2 and HSP-70 in tumour tissues compared to the sham group. Oxaliplatin 28-39 caspase 9 Mus musculus 104-120 35226278-3 2022 Furthermore, 0.5 mM NaF exposure for 24 h exposure increased the proportion of apoptosis and expression of caspase-3 and caspase-9 in mouse spermatocytes (GC-2spd cell line), whereas inhibition of HuR reduced apoptosis and the expression of caspase-3 and caspase-9. Sodium Fluoride 20-23 caspase 9 Mus musculus 121-130 35226278-3 2022 Furthermore, 0.5 mM NaF exposure for 24 h exposure increased the proportion of apoptosis and expression of caspase-3 and caspase-9 in mouse spermatocytes (GC-2spd cell line), whereas inhibition of HuR reduced apoptosis and the expression of caspase-3 and caspase-9. Sodium Fluoride 20-23 caspase 9 Mus musculus 255-264 35126176-11 2021 Levosimendan also maintained mitochondrial membrane potential, decreased cleaved caspase-3 (P = 0.034), cleaved caspase-9 (P < 0.0001), Bax expression (P < 0.0001), and increased Bcl2 expression (P = 0.0036). Simendan 0-12 caspase 9 Mus musculus 112-121 35019826-12 2022 In addition, mitochondrial membrane depolarization, ROS, caspase-3, caspase-9, and apoptosis values induced by MPP decreased with resveratrol treatment. Resveratrol 130-141 caspase 9 Mus musculus 68-77 35013891-5 2022 After different concentration of nano-TiO2 treatments, the cell viability, apoptosis, mitochondrial membrane potential (Deltapsim), BTB junction proteins (Claudin-11, ZO-1, beta-catenin), apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3), and phosphorylated (p)-JNK protein were examined. titanium dioxide 38-42 caspase 9 Mus musculus 236-245 35013891-9 2022 The protein levels of Bax, cleaved caspase-9, and cleaved caspase-3 increased significantly from 150 mug/mL nano-TiO2 group, and the protein level of Bcl-2 decreased significantly from 100 mug/mL nano-TiO2 group. titanium dioxide 113-117 caspase 9 Mus musculus 35-44 35101250-11 2022 The results demonstrated that EGb protection can effectively diminish H2O2-induced apoptosis by inhibiting p53 acetylation, reducing the ratio of Bax/Bcl-2 and suppressing the expression of specific cleavage of Caspase-9 and Caspase-3. Hydrogen Peroxide 70-74 caspase 9 Mus musculus 211-220 35101253-3 2022 In addition, beta-elemene induced nuclear chromatin condensation and cell membrane phosphatidylserine eversion, decreased cell mitochondrial membrane potential, and promoted the cleavage of caspase-3, caspase-9 and PARP proteins, indicating apoptosis in colorectal cancer cells. beta-elemene 13-25 caspase 9 Mus musculus 201-210