PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17349619-5	2007	The mechanisms by which salidroside protected neuron cells from oxidative stress included the induction of several antioxidant enzymes, thioredoxin, heme oxygenase-1, and peroxiredoxin-I; the downregulation of pro-apoptotic gene Bax and the upregulation of anti-apoptotic genes Bcl-2 and Bcl-X(L).	rhodioloside	24-35	BCL2 like 1	Homo sapiens	288-296	
32945356-9	2020	Exposure to ox-LDL induced an increase in the expression of miR-133a, with a concomitant decrease in the level of Bcl-xL in the HCAECs; these effects were reversed by treatment with SAL.	rhodioloside	182-185	BCL2 like 1	Homo sapiens	114-120	
32945356-11	2020	On the whole, the findings of the present study demonstrate that SAL inhibits the ox-LDL-induced upregulation of miR-133a expression, while promoting the expression of Bcl-xL, thereby preventing endothelial cell apoptosis.	rhodioloside	65-68	BCL2 like 1	Homo sapiens	168-174	
20615444-5	2010	The mechanisms of salidroside protected neurons from oxidative stress included the induction of antioxidant enzymes, thioredoxin (Trx), heme oxygenase-1 (HO-1), and peroxiredoxin-I (PrxI); the downregulation of pro-apoptotic protein Bax and the upregulation of anti-apoptotic protein Bcl-X(L).	rhodioloside	18-29	BCL2 like 1	Homo sapiens	284-292	
24471788-9	2014	Additionally, SAL reversed the phosphorylation of JNK and p38 MAPK induced by H2O2 and suppressed the changes in the Bax/Bcl-xL ratio observed after stimulation with H2O2.	rhodioloside	14-17	BCL2 like 1	Homo sapiens	121-127