PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25943027-8	2015	In summary, Sal A attenuates TNF-alpha- and D-GalN-induced both ER stress and mitochondrial-dependent apoptosis by suppression of Bax/Bcl-2 ratio and prevention of calcium release, which support the notion that Sal A could be developed into a novel hepatic protectant.	salvianolic acid	12-17	BCL2 associated X, apoptosis regulator	Homo sapiens	130-133	
30431688-4	2019	SA upregulated the expression levels of Bcl-2 and decreased the levels of Bax, cleaved caspase-3, and cleaved caspase-9.	salvianolic acid	0-2	BCL2 associated X, apoptosis regulator	Homo sapiens	74-77	
25943027-7	2015	Furthermore, the decreased levels of Bax/Bcl-2 ratio and calcium release were measured in Sal A-treated cells.	salvianolic acid	90-95	BCL2 associated X, apoptosis regulator	Homo sapiens	37-40