丁苯酞可通过雷帕霉素靶蛋白信号通路改善心肌梗死大鼠心功能

闫增强.丁苯酞可通过雷帕霉素靶蛋白信号通路改善心肌梗死大鼠心功能[J].内科急危重症杂志,2022,28(4):325-328

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DOI：10.11768/nkjwzzzz20220417

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基金项目:2019年度河北省医学科学研究课题计划（No:20190011)

作者	单位	E-mail
闫增强	沧州市人民医院	kdyon4@163.com

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中文摘要:

目的：探究丁苯酞通过雷帕霉素靶蛋白（mTOR）信号通路对心肌梗死（MI）大鼠心脏功能的影响。方法：将30只雄性大鼠随机分为假手术组（sham组）、MI组和丁苯酞治疗组（NBP组），各10只。检测3组大鼠的心脏功能、左心室质量和左心室指数，采用HE染色和Masson染色观察大鼠心肌组织病理及胶原纤维化情况，采用免疫印迹试验检测mTOR和磷酸化的mTOR（P-mTOR）表达。结果：与sham组比较，MI组大鼠左室舒张末期内径（LVEDD）和左室收缩末期内径（LVESD）明显升高，左室射血分数（LVEF）和左室短轴缩短率（LVFS）水平显著降低（P均<0.05），干预后的NBP组得到明显改善（P均<0.05）。MI组大鼠的左心室质量和左室质量指数明显高于sham组（P均<0.05）；干预后的NBP组大鼠得到显著抑制（P均<0.05）。与sham组比较，MI组大鼠的mTOR和P-mTOR明显减少（P均<0.05）；丁苯酞治疗组大鼠的mTOR和P-mTOR表达显著升高（P均<0.05）。结论：丁苯酞可改善心肌梗死大鼠的心功能，推测是通过激活mTOR信号通路，进而对心功能起到保护作用。

英文摘要:

Objective: To explore the effect of butylphthalide (NBP) on cardiac function in rats with myocardial infarction (MI) through the signal pathway of mammalian target of rapamycin (mTOR). Methods: A total of 30 male rats were divided into sham group, MI group and NBP group. Cardiac function, left ventricular mass and left ventricular index were measured. Myocardial histopathology and collagen fibrosis were observed by HE staining and Masson staining. Western blotting was used to detect the expression of mTOR and phosphorylated mTOR (p-mTOR). Results: As compared with sham group, LVEDD and LVESD were significantly increased, LVEF and LVFS were significantly decreased in MI group (P<0.05), and those in NBP group were significantly improved after intervention (P<0.05). The left ventricular mass and left ventricular mass index in MI group were significantly higher than those in sham group (P<0.05); After intervention, the left ventricular mass and left ventricular mass index in NBP group were significantly inhibited (P<0.05). Compared with sham group, mTOR protein and p-mTOR protein in MI group were significantly decreased (P<0.05). After intervention with NBP, the expression of mTOR protein and p-mTOR protein in NBP group increased significantly (P<0.05). Conclusion: can improve the cardiac function of rats with myocardial infarction. It is speculated that NBP can protect cardiac function by activating mTOR signaling pathway.