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(-)-表没食子儿茶素-3-没食子酸酯减轻糖尿病Goto-Kakizaki大鼠的心肌线粒体功能障碍和自噬。

(-)-Epigallocatechin-3-gallate attenuated myocardial mitochondrial dysfunction and autophagy in diabetic Goto-Kakizaki rats.

作者信息

Liu J, Tang Y, Feng Z, Liu J, Liu J, Long J

机构信息

Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology and Frontier Institute of Life Science, FIST, Xi'an Jiaotong University , Xi'an , P. R. China.

出版信息

Free Radic Res. 2014 Aug;48(8):898-906. doi: 10.3109/10715762.2014.920955. Epub 2014 Jun 4.

Abstract

Type 2 diabetes mellitus (T2DM) is a risk factor for heart disease. However, the mechanisms of T2DM involvement in cardiac complications are still unclear. In the present study, we investigated mitochondria-related mechanisms underlying the pathogenesis of myocardial disorders in diabetic Goto-Kakizaki (GK) rats. We found that remarkable myocardial mitochondrial deficiency and dysfunction as well as oxidative stress occurred in the heart of GK rats. In addition, our results suggested that the loss of mitochondria was in response to elevated autophagy and upstream FoxO factors in diabetic myocardium. More importantly, (-)-epigallocatechin-3-gallate (EGCG), a polyphenol derived from green tea, successfully improved mitochondrial function and autophagy in the heart of GK rats. Our findings revealed that diabetes-associated myocardial mitochondrial deficiency and dysfunction was associated with enhanced autophagy in myocardium, and EGCG might be a potential agent in preventing and treating myocardial disorders involved in diabetes.

摘要

2型糖尿病(T2DM)是心脏病的一个危险因素。然而,T2DM参与心脏并发症的机制仍不清楚。在本研究中,我们调查了糖尿病Goto-Kakizaki(GK)大鼠心肌疾病发病机制中与线粒体相关的机制。我们发现GK大鼠心脏中出现了显著的心肌线粒体缺陷和功能障碍以及氧化应激。此外,我们的结果表明,线粒体的丢失是对糖尿病心肌中自噬增加和上游FoxO因子的反应。更重要的是,(-)-表没食子儿茶素-3-没食子酸酯(EGCG),一种源自绿茶的多酚,成功改善了GK大鼠心脏中的线粒体功能和自噬。我们的研究结果表明,糖尿病相关的心肌线粒体缺陷和功能障碍与心肌中自噬增强有关,并且EGCG可能是预防和治疗糖尿病相关心肌疾病的潜在药物。

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