PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26499133-0	2015	Candesartan ameliorates acute myocardial infarction in rats through inducible nitric oxide synthase, nuclear factor-kappaB, monocyte chemoattractant protein-1, activator protein-1 and restoration of heat shock protein 72.	candesartan	0-11	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	199-220	
26499133-12	2015	Candesartan increased the protein expression of HSP-72 in the acute myocardial infarction rat model.	candesartan	0-11	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	48-54	
26499133-14	2015	These results suggested that candesartan ameliorates acute myocardial infarction in rats through iNOS, NF-kappaB, MCP-1 and AP-1, and the restoration of HSP72.	candesartan	29-40	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	153-158	
21952935-0	2011	Candesartan restored cardiac Hsp72 expression and tolerance against reperfusion injury in hereditary insulin-resistant rats.	candesartan	0-11	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	29-34	
21952935-1	2011	AIMS: We tested the hypothesis that candesartan, an angiotensin II (AII) type 1 receptor antagonist, would restore the depressed phosphatidylinositol 3 (PI3) kinase-dependent Akt phosphorylation, an essential signal to induce heat-shock protein 72 (Hsp72) in response to hyperthermia, in Otsuka Long-Evans Tokushima fatty (OLETF) rats.	candesartan	36-47	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	226-247	
21952935-1	2011	AIMS: We tested the hypothesis that candesartan, an angiotensin II (AII) type 1 receptor antagonist, would restore the depressed phosphatidylinositol 3 (PI3) kinase-dependent Akt phosphorylation, an essential signal to induce heat-shock protein 72 (Hsp72) in response to hyperthermia, in Otsuka Long-Evans Tokushima fatty (OLETF) rats.	candesartan	36-47	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	249-254