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作 者:王飘 郑晴[1] 胡婷 张海银 许言午[1] 包怡敏[1] WANG Piao;ZHENG Qing;HU Ting;ZHANG Hai-yin;XU Yan-wu;BAO Yi-min(School of Basic Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China)
出 处:《中国中医基础医学杂志》2021年第8期1249-1252,1285,共5页JOURNAL OF BASIC CHINESE MEDICINE
基 金:国家自然科学基金青年基金项目(81303256)-基于AMPK-KATP-NF-κB信号通路的三七总皂苷抗心肌缺血再灌注炎症反应的分子机制研究。
摘 要:目的:观察三七总皂苷(PNS)抗心肌缺血再灌注损伤(MIRI)的作用,探讨其对心肌细胞自噬水平的影响。方法:将SD大鼠随机分为假手术组、模型组和模型+三七总皂苷组,采用结扎冠状动脉左前降支后恢复血流灌注建立大鼠心肌缺血再灌注模型。检测血流动力学指标观察大鼠心肌组织病理学变化,检测血清肌钙蛋白含量和心肌组织自噬相关蛋白P62、Beclin-1、LC3Ⅱ蛋白的表达水平。结果:与假手术组比较,模型组的血流动力学指标表现出较为明显的降低趋势(P<0.05),血清肌钙蛋白(cTnT)含量明显升高(P<0.05),自噬相关蛋白Beclin-1、LC3Ⅱ的含量也有明显升高(P<0.05);而使用三七总皂苷预处理后,明显改善MIRI大鼠心肌血流动力学指标降低的趋势(P<0.05),cTnT含量也明显下降(P<0.05);此外PNS预处理后抑制了自噬相关蛋白Beclin-1、LC3II的表达,增加了P62的蛋白表达(P<0.05)。结论:三七总皂苷能有效改善因缺血再灌注所导致的心肌组织损伤,其作用机制可能与调控自噬有关。Objective:To observe the effects of Panax notoginseng saponins(PNS)against myocardial ischemiareperfusion(I/R)injury,and explore its effect on the autophagy of cardiomyocytes.Methods:Rats were randomly divided into three groups:sham,I/R,I/R+PNS.The myocardial I/R model was established by ligating the left anterior descending coronary artery(LAD)for ischemia and reperfusion.The hemodynamic parameters were measured during the ischemia-reperfusion.The pathological changes of rat myocardium were observed,the content of serum troponin T(cTnT)in serum and the expressions of autophagy-related proteins in myocardial tissue were detected.Results:Compared with the sham group,the hemodynamics of the model group was reduced(P<0.05),the serum troponin(cTnT)content was increased significantly(P<0.05),and the autophagy-related proteins Beclin-1 and LC3Ⅱwere also increased(P<0.05).The rats suffered myocardial ischemia-reperfusion injury(MIRI)exhibited improved hemodynamic parameters and a decreased serum cTnT level after PNS pretreatment(P<0.05).Furthermore,PNS pretreatment reduced protein expressions of Beclin-1 and LC3II in the myocardium and increased the protein expression of P62(P<0.05).Conclusion:PNS exhibits cardioprotective effects in MIRI,and the mechanism of this protective effect might be to inhibit autophagy.
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