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

Objective: 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.

Methods: 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.

Results: 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.

Conclusions: Alamandine can protect rat from myocardial IRI via activating JNK phosphorylation and inhibiting NF-κB signaling pathway to reduce the inflammatory response.