PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29955901-10	2018	In addition, TMZ augmented Bcl-2 protein expression and diminished Bax protein expression, the Bax/Bcl-2 rate, and cleaved caspase-3 level.	Trimetazidine	13-16	BCL2 associated X, apoptosis regulator	Rattus norvegicus	95-98	
22282242-17	2012	Furthermore, Western blotting indicated that the expression of anti-apoptotic protein Bcl-2 was up-regulated, while the pro-apoptotic protein Bax was down-regulated in the TMZ+MSCs group, compared with that in the MSCs group.	Trimetazidine	172-175	BCL2 associated X, apoptosis regulator	Rattus norvegicus	142-145	
33704910-0	2021	Trimetazidine improved adriamycin-induced cardiomyopathy by downregulating TNF-alpha, BAX, and VEGF immunoexpression via an antioxidant mechanism.	Trimetazidine	0-13	BCL2 associated X, apoptosis regulator	Rattus norvegicus	86-89	
30780111-6	2019	Administration of the NAR, TMZ, and their combination decreased the plasma level of microRNA-10a, caspase-3, and Bcl-2 associated x protein (Bax) mRNA expression, but increased the B- cell lymphoma 2 (Bcl-2) mRNA expression in the kidney tissue.	Trimetazidine	27-30	BCL2 associated X, apoptosis regulator	Rattus norvegicus	141-144	
30890937-7	2019	Additionally, TMZ ameliorated myocardial injury by inhibiting apoptosis via reducing Bax/Bcl-2 ratio and down-regulating cleaved caspase-3, cleaved PARP, and cytochrome c levels in the myocardium of rats.	Trimetazidine	14-17	BCL2 associated X, apoptosis regulator	Rattus norvegicus	85-88	
29955901-10	2018	In addition, TMZ augmented Bcl-2 protein expression and diminished Bax protein expression, the Bax/Bcl-2 rate, and cleaved caspase-3 level.	Trimetazidine	13-16	BCL2 associated X, apoptosis regulator	Rattus norvegicus	67-70	
30057668-5	2018	After 5 d, post I/R treatment with trimetazidine reduced renal tubular cell necrosis and apoptosis with upregulation of HIF-1alpha-VEGF and tissue inhibitors of metalloproteinase activities, attenuation of matrix metalloproteinase activities, and alteration of the ratio of Bax to Bcl-2 levels.	Trimetazidine	35-48	BCL2 associated X, apoptosis regulator	Rattus norvegicus	274-277	
30203764-12	2018	Trimetazidine can ameliorate rat myocardium following ischemia-reperfusion injury by effectively attenuating the injury from myocardial cell apoptosis; meanwhile, it can resist cell apoptosis through regulating Bax and bcl-2 expression, which exhibits guiding significance for the treatment of myocardial ischemia and reperfusion.	Trimetazidine	0-13	BCL2 associated X, apoptosis regulator	Rattus norvegicus	211-214	
27666568-0	2016	Trimetazidine protects against cardiac ischemia/reperfusion injury via effects on cardiac miRNA-21 expression, Akt and the Bcl-2/Bax pathway.	Trimetazidine	0-13	BCL2 associated X, apoptosis regulator	Rattus norvegicus	129-132	
27666568-7	2016	Furthermore, trimetazidine significantly promoted miRNA-21 expression and phosphorylated-Akt protein expression, and reduced the Bcl-2/Bax ratio in rats following cardiac I/R injury.	Trimetazidine	13-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	135-138	
27666568-10	2016	In addition, trimetazidine exerts protective effects against cardiac I/R injury through cardiac miRNA-21 expression, Akt, and the Bcl-2/Bax pathway.	Trimetazidine	13-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	136-139	
25937560-6	2015	For TMZ-treated cardiomyocytes exposured in hypoxia, we observed a decrease in mRNA expression of proapoptotic Bax, caspase-3 activation and enhanced expression of anti-apoptotic Bcl-2.	Trimetazidine	4-7	BCL2 associated X, apoptosis regulator	Rattus norvegicus	111-114