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

European Review for Medical and Pharmacological Sciences
X-D SongR-X Yang

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 significan...Continue Reading

Citations

May 31, 2020·Cells·Filippo Acconcia

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