PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30575939-16	2018	CONCLUSIONS: Remifentanil can effectively reduce myocardial cell injury caused by myocardial ischemia-reperfusion in rats, improve cardiac function, reduce the myocardial infarction area, decrease cleaved caspase-3 in myocardial cells, and increase Bcl-2/Bax.	Remifentanil	13-25	BCL2, apoptosis regulator	Rattus norvegicus	249-254	
21392805-8	2012	In addition, decrease in Akt, ERK1/2, and Bcl-2, and the increase in Bax by H/R was attenuated by remifentanil-preconditioning (P < 0.05).	Remifentanil	98-110	BCL2, apoptosis regulator	Rattus norvegicus	42-47	
23609459-9	2013	In addition, remifentanil postconditioning enhanced the expression of anti-apoptotic gene Bcl-2 while suppressed the expression of pro-apoptotic gene Bax in hippocampal CA1 region.	Remifentanil	13-25	BCL2, apoptosis regulator	Rattus norvegicus	90-95	
19681651-7	2010	Remifentanil improved expression of ERK1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only.	Remifentanil	0-12	BCL2, apoptosis regulator	Rattus norvegicus	70-74	
19944681-8	2010	Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats.	Remifentanil	0-12	BCL2, apoptosis regulator	Rattus norvegicus	87-92