文章摘要
亓秉超,胡 朗,邱继欢,李春雨,季乐乐,李 妍.人参皂苷Rb1通过上调PGC-1α缓解糖尿病心肌病[J].,2020,(1):19-23
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:2019-06-27  修订日期:2019-07-29
DOI:10.13241/j.cnki.pmb.2020.01.004
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(81570252);国家自然科学基金项目(81770369)
作者单位E-mail
亓秉超 空军军医大学西京医院心内科 陕西 西安 710000 1040132671@qq.com 
胡 朗 空军军医大学西京医院心内科 陕西 西安 710000  
邱继欢 空军军医大学西京医院心内科 陕西 西安 710000  
李春雨 空军军医大学西京医院心内科 陕西 西安 710000  
季乐乐 空军军医大学基础医学院教学实验中心 陕西 西安 710000  
李 妍 空军军医大学西京医院心内科 陕西 西安 710000  
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中文摘要:
      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:采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 caspase-3、bcl-2等蛋白表达;MitoSOX染色分析线粒体ROS含量;透射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,减少了糖尿病小鼠心肌线粒体ROS产生(P<0.01),恢复了bcl-2蛋白表达(P<0.01),降低了cleaved caspase-3蛋白表达(P<0.01),从而减少了高糖引起的细胞凋亡(P<0.05)。而siPGC-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降低心肌线粒体ROS产生并减少心肌细胞凋亡有关。
英文摘要:
      ABSTRACT 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 and DM+Rb1 group. Cardiac function of mice was analyzed by echocardiography. Expression of PGC-1α, cleaved caspase-3 and bcl-2 was analyzed by Western blot. 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). Expression of PGC-1α was down-regulated (P<0.01). 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). The number of mitochondria was increased (P<0.05). At the same time, Rb1 treatment reduced myocardial mitochondrial ROS production (P<0.01), restored bcl-2 protein expression (P<0.01), decreased cleaved caspase-3 protein expression (P<0.01), and decreased Apoptosis induced by high glucose (P<0.05). After treatment with siPGC-1α, the above protective effects of Rb1 were blocked. Conclusion: 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 and reduction of cardiomyocyte apoptosis by ginsenoside Rb1.
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