黄芪甲苷介导SERCA 2a通路改善大鼠心肌缺血再灌注损伤  被引量:7

Astragaloside IV mediates SERCA 2a pathway to improve myocardial ischemia reperfusion injury in rats

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作  者:葛红吉 郭媛利[1] 周南 于洋 GE Hong-ji;GUO Yuan-li;ZHOU Nan;YU Yang(Department of Circulatory and Internal Medicine,Tieling Central Hospital,Tieling 112001;Department of Anesthesiology,General Hospital of the Northern People's Liberation Army,Shenyang 110016,China)

机构地区:[1]辽宁省铁岭市中心医院干部循环内科,辽宁铁岭112001 [2]中国人民解放军北部战区总医院麻醉科,辽宁沈阳110016

出  处:《解剖科学进展》2020年第6期697-700,705,共5页Progress of Anatomical Sciences

基  金:辽宁省自然科学基金(20180551091)。

摘  要:目的探讨黄芪甲苷(Astragaloside IV,AS-IV)对心肌缺血再灌注(Ischemia/reperfusion,I/R)大鼠心肌损伤的保护作用及其可能作用机制。方法将SD大鼠随机分为假手术组(Sham),模型组(I/R)和AS-IV低、高剂量治疗组,每组10只;采用结扎大鼠左冠状动脉前降支的方法制备心肌缺血再灌注模型,并给予黄芪甲苷治疗;HE染色检测大鼠心肌组织病理变化,ELISA法检测大鼠心肌中肌酸激酶(Creatine Kinase,CK)的含量,TUNEL检测大鼠心肌细胞凋亡情况;qPCR和Western blot检测SERCA 2a通路相关蛋白的表达。结果成功制备大鼠心肌缺血在灌注模型;黄芪甲苷明显改善心肌缺血再灌注大鼠心肌组织病理变化,抑制大鼠细胞凋亡,下调心肌组织中肌酸激酶表达,同时上调SERCA 2a蛋白的表达,下调GRP78、ATF-6、PERK的表达,且呈剂量依赖性改变。结论黄芪甲苷改善心肌缺血再灌注大鼠心肌组织损伤,抑制细胞凋亡,与介导SERCA 2a信号通路抑制内质网应激相关。Objective To investigate the protective effect of Astragaloside IV(AS-IV)on myocardial injury induced by myocardial ischemia-reperfusion(I/R)in rats,and to explore its mechanism.Methods SD rats were randomly divided into sham operation group(Sham),model group(I/R)and AS-IV low-and high-dose treatment groups,10 rats in each group.The rats were prepared by ligation of left anterior descending coronary artery in rats.AS-IV was used to treat I/R rats’model;HE staining was used to detect the pathological changes of myocardial tissue in rats.The content of Creatine Kinase(CK)in myocardium was detected by ELISA.The rat cardiomyocytes apoptosis was detected by TUNEL.qPCR and Western blot were used to detect the SERCA 2 a pathway-related protein expression.Results AS-IV significantly improved the pathological changes of myocardial tissue and inhibited the apoptosis in myocardial I/R rats,also downregulated the expression level of creatine kinase,and up-regulated the expression level of SERCA 2 a,down-regulated the expression levels of GRP78,ATF-6,and PERK in a dose-dependent manner.Conclusion AS-IV improved myocardial tissue damage,which is related to the inhibition of apoptosis and endoplasmic reticulum stress via SERCA 2 a signaling pathway in myocardial I/R rats.

关 键 词:黄芪甲苷 心肌缺血再灌注 细胞凋亡 SERCA 2a 内质网应激 大鼠 

分 类 号:R542.2[医药卫生—心血管疾病]

 

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