PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35068334-10 2022 In diabetic thoracic aorta, HG- and CCCP-induced HUVECs, Sal B distinctly increased Bcl-2 expression and reduced BAX, Beclin1, Parkin and Pink1 expression, thereby protecting endothelial cells from apoptosis and mitophagy. salvianolic acid B 57-62 BCL2 apoptosis regulator Homo sapiens 84-89 30204390-10 2016 Conclusion: Sal B is capable of suppressing IHG-induced injury and apoptosis in HUVECs, which might be attributed to the attenuation of oxidative stress, regulation of BCL-2/BAX protein expression, and subsequent suppression of Caspase-3 activity. salvianolic acid B 12-17 BCL2 apoptosis regulator Homo sapiens 168-173 22036624-8 2012 Furthermore, treatment with Sal B down-regulated the IHG-induced release of cytochrome c, AIF nuclear translocation and Bax expression, but mitigated the IHG-mediated down-regulation of BcL-2 expression in SCs. salvianolic acid B 28-33 BCL2 apoptosis regulator Homo sapiens 186-191 22252725-5 2012 Furthermore, Sal B down-regulated the HG-mediated Bax expression and AIF nuclear translocation and the release of cytochrome c, but up-regulated the HG-induced BcL-2 expression in SCs. salvianolic acid B 13-18 BCL2 apoptosis regulator Homo sapiens 160-165