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人参皂苷Rb1通过上调PGC-1α缓解糖尿病心肌病 |
Ginsenoside Rb1 alleviates diabetic cardiomyopathy through up-regulating PGC-1α |
投稿时间:2019-06-10 修订日期:2019-06-10 |
DOI: |
中文关键词: 人参皂苷Rb1 糖尿病心肌病 PGC-1α 线粒体ROS |
英文关键词: Ginsenoside Rb1 Diabetic cardiomyopathy PGC-1α Mitochondrial ROS |
基金项目:国家自然科学基金项目(面上项目,重点项目,重大项目) |
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中文摘要: |
目的:研究人参皂苷Rb1对糖尿病心肌病的治疗作用并阐明其分子机制。方法:用腹腔注射链脲佐菌素的方法,建立糖尿病心肌病动物模型。将小鼠分为3组:WT组,DM组,DM+Rb1组。超声心动图分析小鼠心功能;Western blot分析PGC-1α、cleaved caspase3、bcl2等蛋白表达;MitoSOX染色分析线粒体ROS含量;电镜分析线粒体数目。结果:与WT组相比,DM组小鼠心功能显著下降(LVEF,P<0.01),PGC-1α表达下调(P<0.01),线粒体数目减少(P<0.01);而Rb1处理后,显著改善了DM小鼠心功能(LVEF,P<0.01),恢复了PGC-1α表达(P<0.05),增加了线粒体数目(P<0.05)。同时,Rb1处理后,减少了高糖引起的细胞凋亡(P<0.05)。而siPGCC-1α处理后,阻断了Rb1的上述作用。结论:人参皂苷Rb1通过上调PGC-1α改善糖尿病小鼠心功能,缓解糖尿病心肌病。其机制可能与人参皂苷Rb1减少心肌线粒体ROS产生,抑制caspase3活化和减少心肌细胞凋亡有关。 |
英文摘要: |
Objective: To study the therapeutic effect of ginsenoside Rb1 on diabetic cardiomyopathy and to elucidate its molecular mechanism. Methods: An animal model of diabetic cardiomyopathy was established by intraperitoneal injection of streptozotocin. Mice were divided into 3 groups: WT group, DM group, DM+Rb1 group. The cardiac function of mice was analyzed by echocardiography; the expression of PGC-1α, cleaved caspase3 and bcl2 was analyzed by Western blot; the mitochondrial ROS content was analyzed by MitoSOX staining; the number of mitochondria was analyzed by electron microscopy. Results: Compared with the WT group, the cardiac function of the DM group was significantly decreased (LVEF, P<0.01); the expression of PGC-1α was down-regulated (P<0.01); and the number of mitochondria was decreased (P<0.01). After Rb1 treatment, the cardiac function of DM mice was significantly improved (LVEF, P<0.01); PGC-1α expression was restored (P<0.05); and the number of mitochondria was increased (P<0.05). At the same time, after Rb1 treatment, the apoptosis induced by high glucose was reduced (P<0.05). After treatment with siPGCC-1α, the above protective effects of Rb1 were blocked. Conclusions: Ginsenoside Rb1 improves cardiac function and alleviates diabetic cardiomyopathy by up-regulating PGC-1α. The mechanism may be related to the reduction of myocardial mitochondrial ROS production, inhibition of caspase3 activation and reduction of cardiomyocyte apoptosis after treatment with ginsenoside Rb1. |
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