PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28968609-8 2017 RESULTS: We report that exposure of pancreatic beta-cells to Simvastatin, an inhibitor of mevalonic acid (MVA) biosynthesis, and its downstream isoprenoid derivatives, or FTI-277, an inhibitor of farnesyltransferase that mediates farnesylation of lamins, leads to activation of caspase 3 and lamin B degradation. Simvastatin 61-72 caspase 3 Homo sapiens 278-287 33008033-7 2020 Furthermore, simvastatin 40 mg/kg most profoundly attenuated tubular apoptosis, determined as a decrease of cytochrome C, caspase-3 expression, and AIs (p < 0.01 vs. LPS). Simvastatin 13-24 caspase 3 Homo sapiens 122-131 33008033-8 2020 Conversely, simvastatin induced a significant increase of Bcl-XL and survivin, both in the strong inverse correlations with cleaved caspase-3 and cytochrome C. Simvastatin 12-23 caspase 3 Homo sapiens 132-141 33008033-9 2020 Our study indicates that simvastatin has cytoprotective effects against LPS-induced tubular apoptosis, seemingly mediated by upregulation of cell-survival molecules, such as Bcl-XL and survivin, and inhibition of the mitochondrial cytochrome C and downstream caspase-3 activation. Simvastatin 25-36 caspase 3 Homo sapiens 259-268 32727400-15 2020 However, similar to the effects in A2780 cells, simvastatin and zoledronic acid significantly induced caspase 3/7 activation (6-folds; p < 0.001). Simvastatin 48-59 caspase 3 Homo sapiens 102-113 31839714-7 2019 Results: Both simvastatin and fluvastatin produced a dose- and time-dependent inhibition of cell viability and colony formation while a promotion of cell apoptosis as evident with increases in caspase-3 activity, cleaved-caspase-3, cleaved-caspase-8 and cleaved-PARP levels in PC3 cells. Simvastatin 14-25 caspase 3 Homo sapiens 193-202 31839714-7 2019 Results: Both simvastatin and fluvastatin produced a dose- and time-dependent inhibition of cell viability and colony formation while a promotion of cell apoptosis as evident with increases in caspase-3 activity, cleaved-caspase-3, cleaved-caspase-8 and cleaved-PARP levels in PC3 cells. Simvastatin 14-25 caspase 3 Homo sapiens 221-230 30503138-8 2018 Simvastatin also regulated leiomyoma cell apoptosis through a concentration-dependent increase in activity of caspase-3. Simvastatin 0-11 caspase 3 Homo sapiens 110-119 30038146-7 2018 Results: Results showed that simvastatin alleviates UVB-induced cell death, cell apoptosis, and caspase-3 activity. Simvastatin 29-40 caspase 3 Homo sapiens 96-105 30038146-8 2018 Conclusion: Our findings indicated that simvastatin alleviated UVB-induced corneal endothelial cell apoptosis via caspase-3 activity. Simvastatin 40-51 caspase 3 Homo sapiens 114-123 29664056-14 2018 Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment. Simvastatin 143-154 caspase 3 Homo sapiens 51-60 33174049-0 2020 [Corrigendum] Effects of simvastatin on iNOS and caspase-3 levels and oxidative stress following smoke inhalation injury. Simvastatin 25-36 caspase 3 Homo sapiens 49-58 32633363-11 2020 In addition, simvastatin induced apoptosis of NPC cells and enhanced the Luciferase activity of caspase-3. Simvastatin 13-24 caspase 3 Homo sapiens 96-105 32633363-12 2020 Western blot results indicated that simvastatin promoted the protein level of Bax and caspase-3, whereas suppressed the protein expression of Bcl-2. Simvastatin 36-47 caspase 3 Homo sapiens 86-95 31105786-8 2019 Simvastatin markedly decreased cell viability in a concentration-dependent manner, increased caspase 3 activity and induced apoptosis in C666-1 cells. Simvastatin 0-11 caspase 3 Homo sapiens 93-102 30813251-7 2019 Additionally, COX-2 activity was diminished, and caspase-3 activity was increased to a higher extent by phenothiazine derivative:simvastatin mixtures than by phenothiazine derivatives themselves. Simvastatin 129-140 caspase 3 Homo sapiens 49-58 29532878-8 2018 Simvastatin significantly induced apoptosis, increased the Bax/Bcl-2 ratio, and cleavage of caspase-3 and PARP protein. Simvastatin 0-11 caspase 3 Homo sapiens 92-101 29208461-6 2018 Simvastatin sensitized radioresistance of Ec9706-R cells and suppressed cell proliferation, but aggravated radiation-induced apoptosis and caspase-3 activity. Simvastatin 0-11 caspase 3 Homo sapiens 139-148 29113274-10 2017 Additionally, simvastatin in combination with doxorubicin significantly induced expression of the cyclin-dependent kinase inhibitor p21, increased cytochrome c and caspase 3 expression and reduced cyclin D1 expression. Simvastatin 14-25 caspase 3 Homo sapiens 164-173 26383260-10 2015 In addition, analysis of caspase 3 assays and multiple proteins involved in cellular apoptosis demonstrated that mutant cells were more resistant to simvastatin treatment-induced apoptosis than wild type control cells. Simvastatin 149-160 caspase 3 Homo sapiens 25-34 27109251-7 2016 Pretreatment with KMUP-1, atorvastatin and simvastatin significantly prevented hypoxia-induced EPCs death and apoptosis, with associated increased of the Bcl-2/Bax ratio, and reduced caspase-3 and caspase-9 expression. Simvastatin 43-54 caspase 3 Homo sapiens 183-192 27098189-11 2016 Simvastatin enhanced the release of cytochrome c, caspase 3, and increased p21 levels, especially for the KKU-100 cells. Simvastatin 0-11 caspase 3 Homo sapiens 50-59 26020489-11 2015 Furthermore, the IL-6 receptor blocking antibody tocilizumab was coadministered and unmasked an IL-6-sensitive proportion in the simvastatin-induced caspase 3 activity of metastatic melanoma cells. Simvastatin 129-140 caspase 3 Homo sapiens 149-158 23924855-6 2013 In addition, simvastatin blocked cells in the G1 phase of the cell cycle, downregulated cyclin D1 and CDKs protein expression, mediated the mitochondria-dependent caspase cascade by increasing caspase-3, -8, and -9 mRNA and protein expression, downregulated Xiap levels to induce cells apoptosis. Simvastatin 13-24 caspase 3 Homo sapiens 193-214 25840272-7 2015 Simvastatin induced dose-dependent apoptosis in leiomyoma cells as measured by a fluorometric caspase-3 activity assay, and inhibited proliferation as demonstrated by an (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay (both were significant at 5 and 10 muM). Simvastatin 0-11 caspase 3 Homo sapiens 94-103 25738368-5 2015 In addition, simvastatin arrested cells in the G0/G1 phase of the cell cycle, downregulated the protein expression levels of cyclin D1 and cyclin-dependent kinase (CDK)2, mediated the mitochondria-dependent caspase cascade by increasing the protein expression levels of caspase-3, -8 and -9, and downregulated the protein expression of X-linked inhibitor of apoptosis, which induced cell apoptosis. Simvastatin 13-24 caspase 3 Homo sapiens 270-290 19343037-0 2009 Simvastatin suppresses homocysteine-induced apoptosis in endothelial cells: roles of caspase-3, cIAP-1 and cIAP-2. Simvastatin 0-11 caspase 3 Homo sapiens 85-94 23045963-7 2012 RESULTS AND CONCLUSION: In both GLC-82 and CALU-1 cell lines, simvastatin and R115777 significantly reduced ERK phosphorylation; this effect, which reached the greatest intensity after 36 h treatment, was paralleled by a concomitant induction of apoptosis, documented by significant increase in both caspase-3 activation and TUNEL-positive cells, associated with a reduction in cell numbers. Simvastatin 62-73 caspase 3 Homo sapiens 300-309 22012179-7 2012 A significant, dose-dependent reduction in the expression of caspase-3 and caspase-9 protein induced by H2O2 in MG63 cells was observed in response to simvastatin and the Bcl-2 levels were increased. Simvastatin 151-162 caspase 3 Homo sapiens 61-70 22012179-8 2012 In conclusion, simvastatin protects MG63 cells from oxidative stress-induced apoptosis through downregulation of caspase-3 and caspase-9 activation and upregulation of Bcl-2 expression, suggesting a protective effect in osteoporosis. Simvastatin 15-26 caspase 3 Homo sapiens 113-122 21958871-6 2011 Additionally, simvastatin-induced apoptosis was accompanied by diminished Bcl-2 protein expression, increased cytosolic cytochrome c level, and activation of caspase 9 and caspase 3. Simvastatin 14-25 caspase 3 Homo sapiens 172-181 21477071-6 2011 Western blot analysis showed that procaspase-3 was induced after DCX transfection and activated after simvastatin treatment in YU-PG, HF66, and U87 BTSC. Simvastatin 102-113 caspase 3 Homo sapiens 34-46 20043868-3 2010 Simvastatin induced cardinal features of apoptosis including increased DNA fragmentation, disruption of mitochondrial membrane potential (MMP), and increased caspase-3 activity by depleting isoprenoids in MethA fibrosarcoma cells. Simvastatin 0-11 caspase 3 Homo sapiens 158-167 19934968-8 2009 Simvastatin induced an increase of caspase-3 activity and annexin V staining, and down-regulated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Simvastatin 0-11 caspase 3 Homo sapiens 35-44 19934968-9 2009 Simvastatin also decreased cholesterol content in lipid raft fractions, suppressed caveolin-1 expression in the lipid rafts, and induced Fas translocation into lipid rafts, suggesting that simvastatin may inhibit the prosurvival PI3K/Akt pathway and trigger caspase-3-dependent apoptotic cell death through the modulation of lipid rafts. Simvastatin 0-11 caspase 3 Homo sapiens 258-267 19934968-9 2009 Simvastatin also decreased cholesterol content in lipid raft fractions, suppressed caveolin-1 expression in the lipid rafts, and induced Fas translocation into lipid rafts, suggesting that simvastatin may inhibit the prosurvival PI3K/Akt pathway and trigger caspase-3-dependent apoptotic cell death through the modulation of lipid rafts. Simvastatin 189-200 caspase 3 Homo sapiens 258-267 19934968-10 2009 CONCLUSION: These results suggest that modulation of lipid rafts, Fas translocation, and PI3K/Akt/caspase-3 pathway are involved in the antitumor effect of simvastatin and may have a potential role in cancer prevention and treatment. Simvastatin 156-167 caspase 3 Homo sapiens 98-107 19343037-4 2009 Conversely, simvastatin upregulated c-IAP1 and c-IAP2 expression, while attenuating Hcy-induced apoptosis and caspase-3 activation. Simvastatin 12-23 caspase 3 Homo sapiens 110-119 18203325-8 2008 The apoptosis induced by simvastatin was caspase-3- and caspase-9-dependent. Simvastatin 25-36 caspase 3 Homo sapiens 41-65 18068200-9 2008 Caspase-3/7 activation was inhibited partially by low density lipoprotein (LDL), high density lipoprotein (HDL), z-VAD-fmk (pan-caspase inhibitor), and low doses (0.01 and 0.001 microM) of the cholesterol lowering drug, simvastatin. Simvastatin 220-231 caspase 3 Homo sapiens 0-9 17428261-6 2007 The inhibitory effect of simvastatin on cell proliferation seemed to be associated with cell cycle arrest and increased expression of p21, p27, and activated caspase-3. Simvastatin 25-36 caspase 3 Homo sapiens 158-167 18199714-6 2008 Both lovastatin and simvastatin induced activation of caspase-8, caspase-3, and, to a lesser extent, caspase-9. Simvastatin 20-31 caspase 3 Homo sapiens 65-74 16708807-1 2005 OBJECTIVE: To explore the effect of simvastatin on the cell cycle and caspase-3 expression in human omental preadipocytes. Simvastatin 36-47 caspase 3 Homo sapiens 70-79 17241114-8 2007 Simvastatin pre-treatment resulted in a significant reduction in cytotoxicity (lactate dehydrogenase release and caspase 3 activation) following challenge compared with unchallenged neurons. Simvastatin 0-11 caspase 3 Homo sapiens 113-122 16868926-6 2006 Correspondingly, specific inhibition of cholesterol synthesis in periovulatory human granulosa cells using HMG-CoA reductase inhibitors (lovastatin or simvastatin) increased apoptosis, measured as caspase-3/7 activity. Simvastatin 151-162 caspase 3 Homo sapiens 197-206 16708807-10 2005 CONCLUSION: Simvastatin may block the cells in G0/G1 phase, and induce caspase-3 expression, which may trigger apoptosis. Simvastatin 12-23 caspase 3 Homo sapiens 71-80 15163549-6 2004 Consistent with these data, the activities of caspase-3, caspase-9 and caspase-8 were elevated by simvastatin. Simvastatin 98-109 caspase 3 Homo sapiens 46-55 15949312-6 2005 The level of caspase-3 in EOSs was consistent with the rate of cell apoptosis [(8 +/- 3) microg/L in control, (14 +/- 4), (22 +/- 4), (24 +/- 4), (23 +/- 5) microg/L in 1, 5, 10, 20 micromol/L simvastatin, respectively; compared with control: P = 0.000 - 0.003]. Simvastatin 193-204 caspase 3 Homo sapiens 13-22 15949312-7 2005 However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. Simvastatin 26-37 caspase 3 Homo sapiens 385-394 15949312-7 2005 However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. Simvastatin 115-126 caspase 3 Homo sapiens 385-394 15949312-7 2005 However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. Simvastatin 115-126 caspase 3 Homo sapiens 385-394 15949312-7 2005 However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. Simvastatin 115-126 caspase 3 Homo sapiens 385-394 15949312-7 2005 However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. Simvastatin 115-126 caspase 3 Homo sapiens 385-394 12962723-13 2003 The apoptosis induced by Sim is probably initiated by the mitochondrial caspase 9, which indirectly leads to activation of caspase 3 and 8. Simvastatin 25-28 caspase 3 Homo sapiens 123-132 35269738-7 2022 Simvastatin in a dose of 40 mg/kg showed the most significant effects in amelioration alveolar epithelial cells apoptosis, demonstrating this as a marked decrease of AI (p < 0.01 vs. LPS), cytochrome C, and cleaved caspase-3 expression. Simvastatin 0-11 caspase 3 Homo sapiens 215-224