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Title: [Daphnetin alleviates myocardial ischemia injury in rats through mediating oxidative stress and inhibiting JNK/NF-κB pathway]. Author: Li J, Wang D, Yi L, Li T, Wang M, Zhu H. Journal: Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2020 Jun; 36(6):513-519. PubMed ID: 32696741. Abstract: Objective To study the protective effect and mechanism of daphnetin (DAP) against myocardial ischemia-reperfusion injury in rats. Methods Seventy-five SD rats were randomly divided into five groups: control group, model group, (30, 60, 90) mg/kg DAP-treated groups. The model of myocardial ischemia in rats was established by isoproterenol (85 mg/kg) through subcutaneous injection for 2 consecutive days. DAP was administered by gavage for 7 consecutive days to observe the protective effect of DAP on the injury of rat myocardium. The electrocardiographic changes of each group of experimental rats were measured with electrocardiographic measuring device. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in the sera were detected with spectrophotometry. The serum levels of creatine kinase isoenzyme, muscle b (CK-MB), lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), and the content of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), IL-6 in the homogenate of myocardial tissue were measured by ELISA. The injury and fibrosis of cardiomyocytes were observed by HE staining and Masson staining, the mRNA levels of JNK and NF-κB were detected by real-time quantitative PCR, and the phosphorylation of JNK and NF-κB were determined by Western blot analysis. Results DAP increased the activities of SOD, CAT, GSH-Px, decreased MDA, inhibited the levels of CK-MB, LDH, CPK, TNF-α and IL-β in the sera, decreased myocardial fibrosis, depressed the expression and phosphorylation of JNK and NF-κBp65. Conclusion DAP can inhibit the activation of JNK/NF-κB signal pathway and myocardial apoptosis and fibrosis induced by myocardial ischemia-reperfusion.[Abstract] [Full Text] [Related] [New Search]