Alamandine protects rat from myocardial ischemia-reperfusion injury by activating JNK and inhibiting NF-κB.

Abstract

The aim of this study was to investigate whether alamandine plays a protective role in myocardial ischemia-reperfusion injury (IRI) by activating C-Jun N-terminal kinase (JNK) and inhibiting the expression of key proteins in nuclear factor-kappa B (NF-κB) pathway. Twenty-four Sprague Dawley (SD) rats were numbered and divided into three groups using a random number table, including sham operation group (Sham group), myocardial ischemia-reperfusion injury model group (IRI group), and alamandine pretreatment and myocardial IRI treatment (alamandine group), with 8 SD rats per group. Myocardial tissues were collected from each group. The damage of myocardial tissue was detected using hematoxylin-eosin (H&E) and Masson staining. Finally, the expression levels of JNK and NF-κB pathway-related proteins in myocardial tissue of each group were detected by Western blot. Compared with the IRI group, the alamandine treatment significantly improved cardiac function indicators induced by myocardial IRI in rats, including HR, MAP, LVESP, LVEDP, LVdp/dtmax, and -LVdp/dtmax. In addition, the pathological changes and cell damage of myocardium after alamandine pretreatment were significantly alleviated. At the same time, alamandine can significantly reduce the levels of TNF-α, IL-1β, IL-6, and NO. Finally, Western blot analysis showed that alamandine pre-treatment can protect cardiomyocytes from myocardial IRI by activating JNK phosphorylation and inhibiting the expression of related proteins in the NF-κB signaling pathway. Alamandine can protect rat from myocardial IRI via activating JNK phosphorylation and inhibiting NF-κB signaling pathway to reduce the inflammatory response.