PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33174032-0	2020	Metformin protects high glucose-cultured cardiomyocytes from oxidative stress by promoting NDUFA13 expression and mitochondrial biogenesis via the AMPK signaling pathway.	Metformin	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	147-151	
33174032-3	2020	Metformin, an AMP-activated protein kinase (AMPK) activator, protects cardiomyocytes from oxidative stress by improving mitochondrial function; however, the exact underlying mechanisms are not completely understood.	Metformin	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	14-42	
33174032-3	2020	Metformin, an AMP-activated protein kinase (AMPK) activator, protects cardiomyocytes from oxidative stress by improving mitochondrial function; however, the exact underlying mechanisms are not completely understood.	Metformin	0-9	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	44-48	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	10-19	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	78-82	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	10-19	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	147-151	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	10-19	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	147-151	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	202-211	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	78-82	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	202-211	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	147-151	
33174032-11	2020	Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis.	Metformin	202-211	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	147-151