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首页> 外文期刊>Journal of Cellular Physiology >Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats
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Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

机译:mTOR的影响/ NFκB信号通路和高在心肌胸硬膜外麻醉通过自噬在大鼠缺血再灌注损伤应承担的

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We investigated the role of mammalian target of rapamycin/nuclear factor‐kappa B (mTOR/NF‐κB) signaling pathway in high thoracic epidural anesthesia (HTEA) against myocardial ischemia‐reperfusion (I/R) injury in rats. The rat model of myocardial I/R injury was established. Ninety rats were divided into the normal, sham, I/R, eHTEA, the PDTC, and HTEA?+?PDTC groups. ELISA was applied to detect cardiac function indexes. HE staining was conducted to observe histopathological changes of myocardial tissues, and TTC staining was performed to detect the myocardial infarction size. TUNEL staining was adopted to detect the cell apoptosis rate. The mRNA and protein levels of mTOR, NF‐κB, Fasl, Bcl‐2 and Bax, and LC3‐I, LC3‐II, BNIP3, and Atg5 were detected by RT‐qPCR and Western blotting, respectively. The findings indicated that compared with the normal and sham groups, the I/R, PDTC, and HTEA groups showed the larger myocardial infarction size and increased cell apoptosis rate, while the results in the HTEA?+?PDTC group were opposite. Compared with the normal and sham groups, the I/R group showed reduced mRNA and protein levels of Bcl‐2, LC3, BNIP3, and Atg5, and elevated mRNA and protein levels of mTOR, p50, p65, Bax, and Fasl, while the HTEA?+?PDTC group revealed the opposite results, and the PDTC and HTEA group revealed the increased mRNA and protein levels of Bcl‐2, LC3, BNIP3, Atg5, mTOR, p50, p65, Bax, and Fasl. These results prove that the inhibition of mTOR/NF‐κB signaling pathway potentiates HTEA against myocardial IR injury by autophagy and apoptosis in rats.
机译:我们研究了哺乳动物的目标的作用雷帕霉素/核因子量k B (mTOR / NFκB)应承担的信号通路在胸高硬膜外麻醉对心肌(HTEA)地理缺血再灌注(I / R)损伤的老鼠。心肌I / R损伤的大鼠模型建立。正常的,虚假的,I / R, eHTEA, PDTC,HTEA + ?心脏功能指标。进行观察的组织病理学变化心肌组织,TTC染色执行检测心肌梗死大小。细胞凋亡率。mTOR, NF的‐κB, Fasl Bcl‐2和Bax, LC3‐我,LC3高II BNIP3, Atg5被RT qPCR应承担的检测和免疫印迹。表明,相比正常的和虚假的组I / R, PDTC HTEA组显示较大的心肌梗死大小和增加细胞凋亡率,而导致的HTEA + ?正常的和虚假的团体,I / R组显示信使rna和蛋白质水平降低的Bcl 2,应承担LC3,BNIP3, Atg5,高架信使rna和蛋白质mTOR的水平,p50 p65,伯灵顿,和Fasl,HTEA ? + ?结果,和PDTC HTEA组了信使rna和蛋白质水平的增加Bcl 2,应承担LC3,BNIP3、Atg5 mTOR、p50 p65,伯灵顿,Fasl。结果表明,抑制mTOR / NFκB信号通路强化HTEA反对心肌红外伤自噬和凋亡在老鼠身上。

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