• 中国中文核心期刊
  • 中国科学引文数据库核心期刊
  • 中国科技核心期刊
  • 中国高校百佳科技期刊
高级检索

姜黄素对高糖诱导的L6细胞线粒体功能障碍的改善作用

薛春玲, 诸葛远莉, 曾静霞

薛春玲, 诸葛远莉, 曾静霞. 姜黄素对高糖诱导的L6细胞线粒体功能障碍的改善作用[J]. 中国药科大学学报, 2016, 47(3): 342-347. DOI: 10.11665/j.issn.1000-5048.20160316
引用本文: 薛春玲, 诸葛远莉, 曾静霞. 姜黄素对高糖诱导的L6细胞线粒体功能障碍的改善作用[J]. 中国药科大学学报, 2016, 47(3): 342-347. DOI: 10.11665/j.issn.1000-5048.20160316
XUE Chunling, ZHUGE Yuanli, ZENG Jingxia. Improved effect of curcumin on mitochondrial dysfunction induced by high glucose in L6 cells[J]. Journal of China Pharmaceutical University, 2016, 47(3): 342-347. DOI: 10.11665/j.issn.1000-5048.20160316
Citation: XUE Chunling, ZHUGE Yuanli, ZENG Jingxia. Improved effect of curcumin on mitochondrial dysfunction induced by high glucose in L6 cells[J]. Journal of China Pharmaceutical University, 2016, 47(3): 342-347. DOI: 10.11665/j.issn.1000-5048.20160316

姜黄素对高糖诱导的L6细胞线粒体功能障碍的改善作用

Improved effect of curcumin on mitochondrial dysfunction induced by high glucose in L6 cells

  • 摘要: 考察姜黄素对高糖诱导的L6细胞线粒体功能障碍的改善作用。采用40 mmol/L葡萄糖处理24 h,建立L6细胞线粒体功能障碍模型,姜黄素受试浓度分别为10、20、40 μmol/L。结果显示,高糖培养可引起L6细胞线粒体功能出现明显障碍,主要表现为明显的线粒体膜电位降低、活性氧增多、ATP含量减少,线粒体生物合成(mtDNA数量)部分下降,同时UCP2 、PGC-1α和Sirt3 mRNA和蛋白表达下调。姜黄素对于高糖所致线粒体功能障碍(膜电位下降,活性氧增多、ATP含量减少)具有明显的改善作用,同时升高UCP2的mRNA和蛋白表达,对于线粒体生物合成(mtDNA数量)未见明显影响。本研究提示姜黄素可能是通过多种途径的抗氧化作用而发挥线粒体保护作用。
    Abstract: To investigate the effects of curcumin on mitochondrial dysfunction induced by high glucose(40 mmol/L glucose, 24 h)in L6 cells, curcumin(10, 20, 40 μmol/L)was administered for 24 h after high glucose culture. The effects of curcumin on the mitochondrial dysfunction were evaluated by mitochondrial membrane potential, reactive oxygen species(ROS), ATP content and mtDNA copy number. The mRNA and protein expression of uncoupling protein 2(UCP2), PPARγ coactivator 1α(PGC-1α)and sirtuin-1(Sirt3)were also determined. As improvement of high glucose damage, curcumin significantly raised mitochondrial membrane potential and ATP content, and decreased ROS level. Curcumin significantly ameliorated the down regulation of UCP2 yet with little effect on mtDNA copy number and PGC-1α and Sirt3 expression. In conclusion, curcumin could significantly ameliorate mitochondrial dysfunction in L6 cells induced by high glucose, which involved the mechanism of multiple antioxidants.
  • [1] Patti ME,Corvera S.The role of mitochondria in the pathogenesis of type 2 diabetes[J].Endocr Rev,2010,31(3):364-395.
    [2] Sivitz WI,Yorek MA.Mitochondrial dysfunction in diabetes:from molecular mechanisms to functional significance and therapeutic opportunities[J].Antioxid Redox Signal,2010,12(4):537-577.
    [3] Badin PM,Langin D,Moro C.Dynamics of skeletal muscle lipid pools[J].Trends Endocrinol Metab,2013,24(12):607-615.
    [4] Kelley DE,He J,Menshikova EV,et al.Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes[J].Diabetes,2002,51(10):2944-2950.
    [5] Liu ZH,Yu W,Liu C,et al.Protective effect of curcumin on myocardium in diabetic rats[J].Chin J Pathophysiol(中国病理生理杂志),2014,30(4):725-728.
    [6] Wang ZF,Zhong L.Experimental study on the effects of curcumin on diabetes in rats[J].Chinese J Appl Physiol(中国应用生理学杂志),2014,30(1):66-69.
    [7] Li X,Xu ZM,Jiang ZZ,et al.Hypoglycemic effect of catalpol on high-fat diet/streptozotocin-induced diabetic mice by increasing skeletal muscle mitochondrial biogenesis[J].Acta Biochim Biophys Sin,2014,46(7):738-748.
    [8] Uo JJ,Chang HH,Tsai TH,et al.Positive effect of curcumin on inflammation and mitochondrial dysfunction in obese mice with liver steatosis[J].Int J Mol Med,2012,30(3):673-679.
    [9] Romano AD, Greco E, Vendemiale G, et al. Bioenergetics and mitochondrial dysfunction in aging:recent insights for a therapeutical approach[J].Curr Pharm Design,2014,20(18):2978-2992.
    [10] Newsholme P,Haber EP,Hirabara SM,et al.Diabetes associated cell stress and dysfunction:role of mitochondrial and non-mitochondrial ROS production and activity[J].J Physiol,2007,583(Pt 1):9-24.
    [11] Zephy D,Ahmad J.Type 2 diabetes mellitus:Role of melatonin and oxidative stress[J].Diabetes Metab Synd,2015,9(2):127-131.
    [12] Yoon Y,Galloway CA,Jhun BS,et al.Mitochondrial dynamics in diabetes[J].Antioxid Redox Signal,2011,14(3):429-457.
    [13] Liesa M,Shirihai OS.Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure[J].Cell Metab,2013,17(4):491-506.
    [14] Collins S,Pi J,Yehuda-Shnaidman E.Uncoupling and reactive oxygen species(ROS)—a double-edged sword for β-cell function? “Moderation in all things”[J].Best Pract Res Clin Endocrinol Metab,2012,26(6):753-758.
    [15] Liu C,Lin JD.PGC-1 coactivators in the control of energy metabolism[J].Acta Biochim Biophys Sin,2011,43(4):248-257.
    [16] Park SH,Ozden O,Jiang H,et al.Sirt3,mitochondrial ROS,ageing,and carcinogenesis[J].Int J Mol Sci,2011,12(9):6226-6239.
计量
  • 文章访问数:  1236
  • HTML全文浏览量:  0
  • PDF下载量:  2177
  • 被引次数: 0
出版历程
  • 刊出日期:  2016-06-24

目录

    /

    返回文章
    返回
    x 关闭 永久关闭