PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32781866-9 2021 Abeta and Hcy-induced decrease of cell viability level was increased by MEM treatment although Abeta and Hcy-induced increase of caspase 3, caspase 9, PARP1, TRPA1, TRPM2 and TRPV1 expression levels were decreased by MEM treatments. Homocysteine 105-108 caspase 3 Homo sapiens 129-138 33268288-9 2021 Moreover, western blotting assay revealed that metformin could decrease Hcy-induced expression of Bax and cleaved caspase3, and increase the expression of Bcl-2. Homocysteine 72-75 caspase 3 Homo sapiens 114-122 30315526-15 2019 Catalpol elevated bcl-2 protein expression and reduced bax, caspase-3, -9 protein expressions in the HCY-treated HAECs. Homocysteine 101-104 caspase 3 Homo sapiens 60-73 31586637-11 2019 In addition, OMT reversed the Hcy-induced apoptosis related biochemical changes such as decreased mitochondrial membrane potential and Bcl-2/Bax protein ratio, and increased protein expression of caspase-9 and caspase-3. Homocysteine 30-33 caspase 3 Homo sapiens 210-219 27633052-0 2016 Upregulation of DAPK contributes to homocysteine-induced endothelial apoptosis via the modulation of Bcl2/Bax and activation of caspase 3. Homocysteine 36-48 caspase 3 Homo sapiens 128-137 29124681-7 2018 In astrocytes, QUIN (100 muM) and Hcy (30 muM) induced caspase-3-dependent apoptosis and morphologic alterations through oxidative status imbalance. Homocysteine 34-37 caspase 3 Homo sapiens 55-64 28630659-4 2017 Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspase-3. Homocysteine 23-26 caspase 3 Homo sapiens 250-259 27633052-7 2016 DAPK inhibition may also reverse the effect of Hcy by the upregulation of B cell leukemia/lymphoma 2 (Bcl2) and poly ADP-ribose polymerase, and the downregulation of Bcl2-associated X protein (Bax) and of caspase 3. Homocysteine 47-50 caspase 3 Homo sapiens 205-214 27633052-8 2016 In conclusion, the present study demonstrated that DAPK contributed to the Hcy-induced endothelial apoptosis via modulation of Bcl2/Bax expression levels and activation of caspase 3. Homocysteine 75-78 caspase 3 Homo sapiens 172-181 26263983-9 2015 In addition, overexpression of miR-30b can improve the Hcy-induced apoptosis in HCAECs by downregulating caspase-3 expression. Homocysteine 55-58 caspase 3 Homo sapiens 105-114 22038300-11 2013 The Hcy-induced increase in caspase-3 activity was prevented by DPI and apocynin, suggesting involvement of NOX activity. Homocysteine 4-7 caspase 3 Homo sapiens 28-37 24867323-5 2014 Cell response to homocysteine-induced DNA damage involved the up-regulation of Bax and, at a greater extent, Bcl-2, but not caspase-3, in association with a p53-independent increase of p21 levels; concomitantly, also p16 levels were increased. Homocysteine 17-29 caspase 3 Homo sapiens 124-133 22038300-5 2013 Hcy induced caspase-3 activity and apoptosis; this effect was concentration dependent and maximal after 6-h exposure to 2.5 mM Hcy. Homocysteine 0-3 caspase 3 Homo sapiens 12-21 22222420-7 2012 Expression of cleaved caspase-3 was significantly increased by Hcy, and pretreatment with caspase-3 inhibitor rescued the cell viability by Hcy. Homocysteine 63-66 caspase 3 Homo sapiens 22-31 22038300-5 2013 Hcy induced caspase-3 activity and apoptosis; this effect was concentration dependent and maximal after 6-h exposure to 2.5 mM Hcy. Homocysteine 127-130 caspase 3 Homo sapiens 12-21 22948038-12 2013 Further, E2 decreased Hcy-induced apoptotic death by upregulating the antiapoptotic protein Bcl-2, decreasing cytochrome c release from mitochondria, and attenuating apoptotic cascade activation (Bax, caspase-9, and caspase-3). Homocysteine 22-25 caspase 3 Homo sapiens 216-225 22222420-7 2012 Expression of cleaved caspase-3 was significantly increased by Hcy, and pretreatment with caspase-3 inhibitor rescued the cell viability by Hcy. Homocysteine 140-143 caspase 3 Homo sapiens 22-31 22222420-7 2012 Expression of cleaved caspase-3 was significantly increased by Hcy, and pretreatment with caspase-3 inhibitor rescued the cell viability by Hcy. Homocysteine 140-143 caspase 3 Homo sapiens 90-99 21737932-0 2011 Homocysteine-induced caspase-3 activation by endoplasmic reticulum stress in endothelial progenitor cells from patients with coronary heart disease and healthy donors. Homocysteine 0-12 caspase 3 Homo sapiens 21-30 22204864-5 2012 Both Hcy and ADA significantly increased PS exposure (n=5), caspase-3 activity (n=6) and cytochrome c release (n=3). Homocysteine 5-8 caspase 3 Homo sapiens 60-69 20305681-11 2010 Furthermore, Hcy caused a significant downregulation of eNOS mRNA, p-eNOS, and p-Akt protein expression as well as an upregulation of p-p38MAPK protein expression and caspase-3 activity. Homocysteine 13-16 caspase 3 Homo sapiens 167-176 21737932-2 2011 Our results indicate that 500 micromol/L homocysteine induced endothelial progenitor cell apoptosis and activation of caspase-3, both of which were abolished by 100 micromol/L and 200 micromol/L salubrinal, an agent that prevents endoplasmic reticulum stress-induced apoptosis. Homocysteine 41-53 caspase 3 Homo sapiens 118-127 21737932-5 2011 These findings suggest that homocysteine induces endoplasmic reticulum stress-mediated activation of caspase-3 in endothelial progenitor cells, an event that is enhanced in patients with coronary heart disease. Homocysteine 28-40 caspase 3 Homo sapiens 101-110 20216988-7 2010 Our results indicate that homocysteine releases Ca(2+) from agonist sensitive stores, enhances eIF2alpha phosphorylation at Ser(51) and activates caspase-3 and -9 independently of extracellular Ca(2+). Homocysteine 26-38 caspase 3 Homo sapiens 146-162 20216988-8 2010 Homocysteine induced activation of caspase-3 and -9 was abolished by salubrinal, an agent that prevents endoplasmic reticulum (ER) stress-induced apoptosis. Homocysteine 0-12 caspase 3 Homo sapiens 35-51 18766198-8 2009 Our in vitro work shows that Hcy-mediated EPC toxicity is due to apoptosis involving caspase-8, cytochrome c release, and caspase-3 activation. Homocysteine 29-32 caspase 3 Homo sapiens 122-131 19343037-5 2009 Hcy may induce HUVEC apoptosis through a pathway involving caspase-3. Homocysteine 0-3 caspase 3 Homo sapiens 59-68 18766198-9 2009 Vitamin B(6), and B(9) significantly impair Hcy-mediated EPC caspase-3 activation in vitro. Homocysteine 44-47 caspase 3 Homo sapiens 61-70 16884727-7 2007 Homocysteine treatment significantly increased caspase-3 activity whereas HDL significantly decreased it as compared to the homocysteine-only treated group. Homocysteine 0-12 caspase 3 Homo sapiens 47-56 18430556-5 2008 When cells were cotreated with homocysteine and Abeta, caspase-3 activity was significantly increased, and expressions of BiP and the spliced form of XBP-1 mRNAs were significantly induced. Homocysteine 31-43 caspase 3 Homo sapiens 55-64 18430556-6 2008 The neurotoxicity of homocysteine was attenuated by the treatment of cells with folate, as determined by caspase-3 activity and apoptotic body staining. Homocysteine 21-33 caspase 3 Homo sapiens 105-114 17149372-6 2007 In addition to increases in pro-caspase-3 protein and caspase-3 activity, cells exposed to Hcy manifested enhanced reactive oxygen species content. Homocysteine 91-94 caspase 3 Homo sapiens 54-63 16967206-5 2007 Both flow cytometric analysis and caspase-3 activity assay showed an increased rate of apoptosis in Hcy-treated lymphocyte cultures compared to controls. Homocysteine 100-103 caspase 3 Homo sapiens 34-43 15561702-3 2005 Our data demonstrated that HCy caused caspase-dependent apoptosis in cultured human umbilical vein endothelial cells, as determined by cell viability, nuclear condensation, and caspase-3 activation and activity. Homocysteine 27-30 caspase 3 Homo sapiens 177-186 16644300-8 2006 In addition, Hcy increased cytochrome c release into the cytosol, and activated caspase-9 and caspase-3, but not caspase-8, indicating that Hcy induces apoptosis via the mitochondria pathway. Homocysteine 13-16 caspase 3 Homo sapiens 94-103 16644300-11 2006 PDTC blocked Hcy-induced caspase-3 activation and apoptosis. Homocysteine 13-16 caspase 3 Homo sapiens 25-34 15211800-6 2004 Hcy-induced HUVEC apoptosis was accompanied by an increased level of caspase3 expression and activation, together with decreased c-IAP2 level. Homocysteine 0-3 caspase 3 Homo sapiens 69-77 15211800-8 2004 CONCLUSION: Hcy may induce HUVEC apoptosis via a pathway involving caspase3, which can be partially antagonized by folic acid, possibly through upregulated c-IAP2 expression. Homocysteine 12-15 caspase 3 Homo sapiens 67-75 11447214-2 2001 In this study, homocysteine induced programmed cell death in human umbilical vein endothelial cells as measured by TdT-mediated dUTP nick end labeling assay, DNA ladder formation, induction of caspase 3-like activity, and cleavage of procaspase 3. Homocysteine 15-27 caspase 3 Homo sapiens 193-202 11447214-2 2001 In this study, homocysteine induced programmed cell death in human umbilical vein endothelial cells as measured by TdT-mediated dUTP nick end labeling assay, DNA ladder formation, induction of caspase 3-like activity, and cleavage of procaspase 3. Homocysteine 15-27 caspase 3 Homo sapiens 234-246 11432446-0 2001 Homocysteine thiolactone induces apoptotic DNA damage mediated by increased intracellular hydrogen peroxide and caspase 3 activation in HL-60 cells. Homocysteine 0-12 caspase 3 Homo sapiens 112-121 35356883-8 2022 Results Compared with those in the control group, the expressions of caspase-3 and circRNA CPSF6 mRNA in the Hcy treatment group significantly increased. Homocysteine 109-112 caspase 3 Homo sapiens 69-78