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首页> 外文期刊>American Journal of Translational Research >Osthole attenuates myocardial ischemia/reperfusion injury in rats by inhibiting apoptosis and inflammation
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Osthole attenuates myocardial ischemia/reperfusion injury in rats by inhibiting apoptosis and inflammation

机译:Osthole通过抑制细胞凋亡和炎症减轻大鼠心肌缺血/再灌注损伤

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摘要

This study was performed to evaluate the cardioprotective effects of osthole (OST) in a rat model of myocardial ischemia/reperfusion injury (MI/RI) and the underlying mechanism. We exposed rat hearts to left anterior descending coronary artery ligation for 30 min followed by 24 h of reperfusion. The results showed that pretreatment with OST ameliorated MI/RI as evidenced by histopathological examination. Moreover, the terminal deoxynucleotidyl transferase dUTP nick end-labeling assay demonstrated that OST suppressed myocardial apoptosis, which may be related to an increase in the Bcl-2/Bax ratio and inhibition of caspase-3 and caspase-9 activation. Furthermore, we determined that OST ameliorated impaired mitochondrial morphology and the oxidation system; OST also attenuated levels of pro-inflammatory cytokines, including tumor necrosis factor α and interleukins 6 and 1β. In conclusion, OST exerted a strong favorable cardioprotective effect on MI/RI, possibly by suppressing the inflammatory response and inhibiting cell apoptosis.
机译:进行这项研究以评估osthole(OST)在心肌缺血/再灌注损伤(MI / RI)大鼠模型中的心脏保护作用及其潜在机制。我们将大鼠心脏暴露于左前冠状动脉前降支结扎30分钟,然后再灌注24 h。结果表明,通过组织病理学检查可知,用OST预处理可改善MI / RI。此外,末端脱氧核苷酸转移酶dUTP缺口末端标记测定法表明OST抑制了心肌细胞凋亡,这可能与Bcl-2 / Bax比值的增加以及caspase-3和caspase-9激活的抑制有关。此外,我们确定OST改善了受损的线粒体形态和氧化系统。 OST还减弱了促炎性细胞因子的水平,包括肿瘤坏死因子α和白介素6和1β。总之,OST可能通过抑制炎症反应和抑制细胞凋亡而对MI / RI发挥了良好的心脏保护作用。

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