PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16995309-15	2006	CONCLUSION: Both Atenolol and Metoprolol treatment can reduce cardiomyocyte apoptosis in infarction/scar, border and non-infarcted areas after AMI, mainly through the increase of bcl-2 expression and bcl-2/bax ratio.	Metoprolol	30-40	BCL2 associated X, apoptosis regulator	Rattus norvegicus	206-209	
17961425-7	2007	(4) The expression level of bax protein was significantly lower in metoprolol group while bcl-2/bax significantly higher than those in placebo group.	Metoprolol	67-77	BCL2 associated X, apoptosis regulator	Rattus norvegicus	28-31	
34765006-20	2021	LVIDd and Bax decreased in the metoprolol group (P < 0.01, P < 0.05), and the Bcl-2/Bax ratio increased (P < 0.05).	Metoprolol	31-41	BCL2 associated X, apoptosis regulator	Rattus norvegicus	10-13	
34765006-20	2021	LVIDd and Bax decreased in the metoprolol group (P < 0.01, P < 0.05), and the Bcl-2/Bax ratio increased (P < 0.05).	Metoprolol	31-41	BCL2 associated X, apoptosis regulator	Rattus norvegicus	84-87	
12738230-8	2003	Metoprolol treatment resulted in: (1) improved LV remodeling (P &lt; 0.025), (2) reduced myocardial apoptosis (P &lt; 0.005), and (3) selective reduction in myocardial Bcl-X(S) expression (P &lt; 0.001) without change in Fas, Fas ligand, Bax, Bcl-2, or Bcl-X(L).	Metoprolol	0-10	BCL2 associated X, apoptosis regulator	Rattus norvegicus	238-241