Arctiin protects rat heart against ischemia/reperfusion injury via a mechanism involving reduction of necroptosis

European Journal of Pharmacology
Heng ChenJun Peng

Abstract

RIPK1/RIPK3/MLKL (Receptor-interacting protein kinase 1/Receptor-interacting protein kinase 3/Mixed lineage kinase domain-like protein) pathway-mediated necroptosis contributes to myocardial ischemia/reperfusion (I/R) injury, and Arctiin can prevent myocardial fibrosis and hypertrophy. This study aims to explore the effect of Arctiin on myocardial I/R injury and the underlying mechanisms. SD rat hearts or cardiomyocytes were subjected to I/R or hypoxia/reoxygenation (H/R) to establish the I/R or H/R injury model. The methods of biochemistry, PI/DAPI (propidium iodide/4',6-Diamidino-2-Phenylindole) and H&E (Hematoxylin & eosin) staining were used to evaluate the I/R or H/R injury. The effects of Arctiin on necroptosis in I/R-treated hearts or H/R-treated cardiomyocytes were assessed. The results showed that Arctiin reduced myocardial I/R injury (decreases in myocardial infarction and creatine kinase release), concomitant with a decrease in levels of necroptosis-associated proteins (RIPK1/p-RIPK1, RIPK3/p-RIPK3 and MLKL/p-MLKL) in I/R-treated rat hearts. Consistently, the necrosis and LDH release in H/R-treated cardiomyocytes were attenuated in the presence of Arctiin, accompanied by suppression of necroptosis-relevant proteins. ...Continue Reading

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