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Protective Effect of Cordycepin on Impairment of Endothelial Function in Type 2 Diabetes Mellitus

文献类型： 外文期刊

作者： Xue, Bei 1 ; Li, Liang 1 ; Gu, Xue-Dong 1 ; Luo, Zhang 1 ; Jia, Fu-Chen 1 ; Zhang, Jia-Chen 1 ; Liu, Yi 1 ; Liu, Zhen-Dong 1 ; Wang, Wen-Han 2 ;

作者机构： 1.Tibet Agr & Anim Husb Univ, Food Sci Coll, Nyingchi Tibet 860000, Peoples R China

2.Shanghai Acad Agr Sci, Shanghai Key Lab Agr Genet & Breeding, Key Lab Appl Mycol Resources & Utilizat, Natl Engn Res Ctr Edible Fungi,Minist Agr,Inst Ed, Shanghai 201403, Peoples R China

关键词： type 2 diabetes mellitus; cordycepin; sirtuin protein 3; mitochondria; vascular relaxation; molecular docking; medicinal mushrooms

期刊名称：INTERNATIONAL JOURNAL OF MEDICINAL MUSHROOMS （ 影响因子：1.706； 五年影响因子：1.817 ）

ISSN： 1521-9437

年卷期： 2022 年 24 卷 3 期

页码：

收录情况： SCI

摘要： Type 2 diabetes mellitus (T2DM) is a major risk factor for cardiovascular diseases. The reduction of mitochondrial protein sirtuin protein 3 (SIRT3) has been reported to contribute to the development of T2DM by impacting mitochondrial respiration. Cordycepin is an adenosine derivative and is isolated from the culture filtrate of Cordyceps militar is. This study explored the protective effect of cordycepin on vascular impairment induced by T2DM and its properties and protective mechanism. In this study, a T2DM rat model was established. The endothelium-dependent relaxation of the thoracic aorta ring decreased in T2DM rats could be reversed by cordycepin. Next, mitochondrial impairment in human umbilical vein endothelial cells was detected by JC-1 staining. In vitro studies revealed that cordycepin plays a beneficial role in advanced glycation end product-induced endothelial mitochondrial impairment. Moreover, according to the cordycepin molecular docking analysis, cordycepin can bind to SIRT3. Cordycepin increased the expression and activation of SIRT3 in a dose-dependent manner. SIRT3 interruption blocked the protective effect of cordycepin on mitochondria in human umbilical vein endothelial cells. Cordycepin can conclusively protect vascular function impaired by T2DM, and the mechanism may potentially be involved in SIRT3 signaling pathways.

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