益母草碱对高糖诱导的人脐静脉内皮细胞线粒体分裂及其功能的影响-现代医学

益母草碱对高糖诱导的人脐静脉内皮细胞线粒体分裂及其功能的影响

单位：上海交通大学医学院附属新华医院老年医学科, 上海 200092

分类号：R329.28

出版年·卷·期（页码）：2018·46·第六期（687-691）

摘要：

目的：探讨益母草碱对高糖诱导的人脐静脉内皮细胞（HUVECs）线粒体分裂及其功能的影响。方法：将HUVECs分为正常糖组、高糖组、益母草碱+高糖组、Mdivi-1+高糖组，采用罗丹明123法检测内皮细胞线粒体功能，Mitotracker染色评价线粒体分裂情况，定量PCR检测细胞基因表达情况，蛋白质印迹法检测细胞中Drp1的蛋白表达水平。结果：与正常糖组比较，高糖组细胞线粒体功能明显降低，线粒体分裂明显增加，Drp1的基因和蛋白表达水平明显增高。与高糖组比较，益母草碱+高糖组细胞线粒体功能明显增强，细胞分裂明显减少，Drp1的基因和蛋白表达水平明显降低。线粒体分裂抑制剂Mdivi-1+高糖组，效果与益母草碱+高糖组类似。结论：益母草碱可能通过调控Drp1依赖的线粒体分裂保护内皮细胞线粒体功能。

Objective:To investigate the effects of Leonurine on mitochondrial mitochondrial division and function of human umbilical vein endothelial cells (HUVECs) induced by high glucose. Methods:The HUVECs were divided into normal glucose group, high glucose group, Leonurine+high glucose group, Mdivi-1+high glucose group, mitochondrial function of endothelial cells was detected by rhodamine 123 method, mitochondrial mitosis was evaluated by Mitotracker staining, Western blotting was used to detect the protein expression level of Drp1 in the cells. Results:Compared with the normal glucose group, the mitochondrial function of high glucose group was significantly decreased, the mitochondrial division increased obviously, and the gene and protein expression of Drp1 was significantly increased. Compared with high glucose group, the activity of mitochondria in Leonurine+high glucose group was significantly increased, cell division was significantly reduced, and Drp1 gene and protein expression levels were significantly reduced. Similar effects were observed inMdivi-1+high glucose group. Conclusion:Leonurine may protect endothelial cell mitochondrial function by regulating Drp1-dependent mitochondrial division.

参考文献：

[1] 刘洁,王尧. 血糖波动与糖尿病并发症的关系[J].现代医学,2010,38(2):200-203.
[2] 朱海燕,王宇光,马增春. 丹参酮ⅡA(TanⅡA)对内皮细胞的氧化损伤及凋亡的影响[J].中药药理与临床,2017,33(1):41-45.
[3] JHENG H F, TSAI P J, GUO S M, et al. Mitochondrial fission contributes to mitochondrial dysfunction and insulin resistance in skeletal muscle[J]. Mol Cell Biol, 2012,32(2):309-319.
[4] QI J, HONG Z Y, XIN H, et al. Neuroprotective effects of leonurine on ischemia/reperfusion-induced mitochondrial dysfunctions in rat cerebral cortex[J]. Biol Pharm Bull, 2010, 33(12):1958-1964.
[5] LIU X H, PAN L L, GONG Q H, et al. Leonurine (SCM-198) improves cardiac recovery in rat during chronic infarction[J]. Eur J Pharmacol, 2010, 649(1-3):236-246.
[6] 黄震浩,魏昕,张琳琳. 益母草碱对高糖诱导的人脐静脉内皮细胞凋亡的抑制作用[J]. 中国医药,2017,12(9):1410-1414.
[7] 庄心宇, 高秀芳, 施海明. 红景天苷对高糖诱导的血管平滑肌细胞中线粒体过度分裂的作用及机制[J].中西医结合心脑血管病杂志,2017,15(1):29,33-36.
[8] 张爽, 袁杰.糖代谢异常与冠心病关系的研究现状[J].东南大学学报:医学版,2016,35(4):602-606.
[9] LIU X H, PAN L L, CHEN P F. Leonurine improves ischemia-induced myocardial injury through antioxidative activity[J]. Phytomedicine, 2010,17(10):753-759.
[10] ZHAN M, BROOKS C, LIU F. Mitochondrial dynamics:regulatory mechanisms and emerging role in renal pathophysiology[J]. Kidney Int, 2013, 83(4):568-581.
[11] de ARRIBA G, CALVINO M, BENITO S. Cyclosporine A-induced apoptosis in renal tubular cells is related to oxidative damage and mitochondrial fission[J]. Toxicol Lett, 2013, 218(1):30-38.
[12] LI J, DONATH S, LI Y. miR-30 regulates mitochondrial fission through targeting p53 and the dynamin-related protein-1 pathway[J]. PLoS Genet, 2010, 6(1):e1000795.
[13] OKADA M,MORIOKA S,KANAZAWA H,et al. Canstatin inhibits isoproterenol-induced apoptosis through preserving mitochondrial morphology in differentiated H9c2 cardiomyoblasts[J]. Apoptosis, 2016,21:887-895.
[14] XIN H, GU M, WANG W W. Effects of leonurine on L-type calcium channel in rat ventricular myocytes[J]. Biol Pharm Bull, 2012,35(8):1249-1256.

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