PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22485212-4 2011 H(2)S-induced cell apoptosis was accompanied by activation of caspase-3 and caspase-9. Hydrogen Sulfide 0-5 caspase 3 Homo sapiens 62-71 28738323-5 2017 RESULTS: H2S attenuated FFA-induced cell apoptosis, and reduced the expression of NLRP3, ASC, pro-caspase-1, caspase-1, IL- 1beta, IL-18 and caspase-3. Hydrogen Sulfide 9-12 caspase 3 Homo sapiens 141-150 26546573-10 2015 CONCLUSIONS: The protective effects of H2S are mediated by thiosulfate that is transported across cell membrane by NaS-2 and exerts antiapoptotic effects via persulfidation of caspase-3. Hydrogen Sulfide 39-42 caspase 3 Homo sapiens 176-185 25738635-10 2015 Treatment of PLC/PRF/5 hepatoma cells with 500 micromol/l NaHS (a donor of H2S) for 24 h markedly increased the expression levels of CSE, CBS, p-IkappaB and NF-kappaB activation, leading to COX-2 and MMP-2 overexpression, and decreased caspase-3 production, as well as increased cell viability and decreased number of apoptotic cells. Hydrogen Sulfide 75-78 caspase 3 Homo sapiens 236-245 23660955-10 2013 Moreover, H2S reduced the expression of the cleaved caspase-3, NOX4 and the leakage of cyt c from the mitochondria to the cytoplasm. Hydrogen Sulfide 10-13 caspase 3 Homo sapiens 52-61 23020085-7 2012 However, the activity of caspase-3 increased in the hypoxic bystander cells, and this could be regulated by both NaHS and the inhibitor of endogenous H(2)S. Hydrogen Sulfide 150-155 caspase 3 Homo sapiens 25-34 18373739-8 2008 H(2)S-induced apoptosis led to an increase in caspase 3 activity and this activity was attenuated when caspase 3 inhibitor were used. Hydrogen Sulfide 0-5 caspase 3 Homo sapiens 46-55 18373739-8 2008 H(2)S-induced apoptosis led to an increase in caspase 3 activity and this activity was attenuated when caspase 3 inhibitor were used. Hydrogen Sulfide 0-5 caspase 3 Homo sapiens 103-112 31443288-4 2019 Cell death induced by H2O2 treatment could be significantly attenuated by the pre-treatment of H2S, resulting in a decrease in the Bax/Bcl-2 ratio and the inhibition of caspase-3 activity in human lung epithelial cell line A549 cells. Hydrogen Sulfide 95-98 caspase 3 Homo sapiens 169-178 16597918-5 2006 Treatment with inhibitors of caspase-3, -8, and -9 significantly inhibited H(2)S-induced phosphatidylserine externalization as shown by reduced annexin V staining. Hydrogen Sulfide 75-80 caspase 3 Homo sapiens 29-50 16446703-0 2006 Hydrogen sulfide prevents apoptosis of human PMN via inhibition of p38 and caspase 3. Hydrogen Sulfide 0-16 caspase 3 Homo sapiens 75-84 15371330-0 2004 Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3. Hydrogen Sulfide 0-16 caspase 3 Homo sapiens 130-139 15371330-7 2004 The activation of ERK by H2S in HASMCs was accompanied by increased caspase-3 activity. Hydrogen Sulfide 25-28 caspase 3 Homo sapiens 68-77 15371330-8 2004 Inhibition of caspase-3 by AC-DEVD-CHO attenuated the H2S-induced cell apoptosis. Hydrogen Sulfide 54-57 caspase 3 Homo sapiens 14-23 15371330-11 2004 Of the three investigated MAPKs, only ERK played an active role in mediating H2S-induced apoptosis of HASMCs by activating caspase-3. Hydrogen Sulfide 77-80 caspase 3 Homo sapiens 123-132 30456731-11 2019 Moreover, H2S could significantly decrease caspase-3 and GFAP-positive cells in the CA1 region of the hippocampus (P < 0.01) compared to the METH group. Hydrogen Sulfide 10-13 caspase 3 Homo sapiens 43-52 30129387-4 2018 The results indicate that NaHS (an H2S donor) administration in uranium-intoxicated kidney cells ameliorated uranium-induced reactive oxygen species generation, caspase-3-dependent apoptosis, and endoplasmic reticulum (ER) stress identified through several key markers including GRP78, C/EBP homologous protein (CHOP), and caspase-12. Hydrogen Sulfide 35-38 caspase 3 Homo sapiens 161-170