PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29688912-7 2018 TLMs are highly efficient hydrogen peroxide scavengers and the activity of caspase-3 inhibition, thereby protecting cells from H/R-induced cytotoxicity. r 129-130 caspase 3 Homo sapiens 75-84 15309413-16 2004 Our results suggest that p38 has a pro-apoptotic role while JNK phosphorylation is protective in our cell model and that these kinases act via caspase-3 to prevent or promote cell survival in response to SI/R-induced injury. r 207-208 caspase 3 Homo sapiens 143-152 31173173-11 2019 In addition, AG490 and S1491 were also identified to alleviate the H/R-induced apoptosis by inhibiting caspase 3 activity and modulating the expression levels of cleaved caspase-3, tumor necrosis factor receptor superfamily member 6 (Fas), Fas ligand, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein. r 69-70 caspase 3 Homo sapiens 103-112 29434685-7 2018 Additionally, pretreatment with SAL reversed the H/R-induced decrease in cellular viability, increased caspase-3 activity, the appearance of apoptotic cells and the apoptosis rate in HBVSMCs. r 51-52 caspase 3 Homo sapiens 103-112 26859194-6 2016 The results showed that IsoRN can reduce A/R-induced injury by decreasing the level of lactate dehydrogenase and creatine phosphokinase release from the cardiomyocytes, increasing cell viability and expression of SIRT1, reducing the generation of reactive oxygen species, inhibiting opening of mitochondrial permeability transition pores and loss of Deltapsim and activation of caspase-3, and decreasing the release of cytochrome c, and reducing apoptosis. r 27-28 caspase 3 Homo sapiens 378-387 22472696-4 2012 RESULTS: H-R caused a significant increase in caspase-3 activity compared with controls in both cell types. r 0-1 caspase 3 Homo sapiens 46-55 30046375-8 2018 Mechanistic experiments revealed that H/R did not influence BDNF, JNK, and caspase 3 expression, but upregulated pro-BDNF, p75NTR, sortilin, phospho-JNK, and cleaved caspase 3 protein levels. r 40-41 caspase 3 Homo sapiens 166-175 30046375-9 2018 In contrast, neutralization of endogenous pro-BDNF with an antibody significantly attenuated H/R-induced upregulation of pro-BDNF, p75NTR, sortilin, p-JNK, and cleaved caspase 3 protein levels, indicating that p75NTR-sortilin signaling and activation of JNK and caspase 3 may be involved in these effects. r 95-96 caspase 3 Homo sapiens 168-177 30046375-9 2018 In contrast, neutralization of endogenous pro-BDNF with an antibody significantly attenuated H/R-induced upregulation of pro-BDNF, p75NTR, sortilin, p-JNK, and cleaved caspase 3 protein levels, indicating that p75NTR-sortilin signaling and activation of JNK and caspase 3 may be involved in these effects. r 95-96 caspase 3 Homo sapiens 262-271 30046375-10 2018 In conclusion, H/R-induced injury may be mediated by pro-BDNF, at least in part through the regulation of p75NTR-sortilin signaling and activation of JNK and caspase 3. r 17-18 caspase 3 Homo sapiens 158-167 27248986-8 2016 AR also inhibited H/R-induced release of mitochondrial cytochrome c and decreased the expression of the caspase-3, Bax proteins. r 1-2 caspase 3 Homo sapiens 104-113