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银杏内酯B对高糖培养的SH-SY5Y细胞线粒体功能的影响

Effect of ginkgolide B on mitochondria function of SH-SY5Y cells incubated with high glucose
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摘要 目的观察银杏内酯B(ginkgolide B,GB)对体外培养的SH-SY5Y细胞线粒体功能的影响。方法高浓度葡萄糖作用于SH-SY5Y细胞建立体外凋亡模型,予以不同浓度GB预处理细胞,流式细胞仪检测细胞凋亡。在高糖培养细胞前,予以40μmol/LGB或培养基预处理细胞6h,流式细胞仪检测线粒体内活性氧(reactive oxygen species,ROS)、线粒体膜电位,分光光度计检测线粒体呼吸链复合物I和Ⅲ活性。结果除了5μmol/L外,其他浓度的GB均可减少高糖引起的细胞凋亡(P〈0.01)。GB组线粒体特异性产生的ROS较高糖组明显减少(P〈0.01),线粒体呼吸链复合物I[(69.2±2.7)VS(51.6±2.9)](P〈0.01)和复合物Ⅲ活性提高[(32.3±2.4)VS(26.2±2.5)](P〈0.05)。同时GB组线粒体膜电位去极化较高糖组减少[(5.8±0.6)vs(3.1±0.6)](P〈0.01)。结论GB可通过保护线粒体功能,抑制ROS产生,减少高糖引起的凋亡细胞。 Objective To investigate the effects of ginkgolide B (GB) on mitochondria function of SH-SY5Y cells incubated with high glucose. Methods SH-SY5Y cells were pre-treated with different concentrations of GB or placebo in vitro, prior to administration of high concentration glucose in order to inducing apoptosis. Cell apoptosis was investigated with flow cytometry. In addition, mitochondrial membrane potential, mitochondrially generated reactive oxygen species (ROS), mitochondrial complexes I and III activity were studied, in order to explore the molecular mechanism of GB. Results GB decreased apoptotic cells (P〈 0.01 ), improved the activity of mitochondria complex I [ (69.2±2.7) vs (51,6±2.9) ] (P〈0.01) and m [ (32.3±2.4) vs (26.2±2.5) ] (P〈0.05), reduced mitochondrially generated ROS production (P〈0.01), relieved mitochondrial potential depolarization induced by high glucose [(5.8±0.6) vs (3.1±0.6) (P〈0.01). Conclusions GB may decrease cell apoptosis induced by high glucose by reliving mitochondria malfunction related to ROS.
出处 《国际麻醉学与复苏杂志》 CAS 2014年第5期426-430,共5页 International Journal of Anesthesiology and Resuscitation
基金 国家自然科学基金(81271390) 广东省自然科学基金(s2011010004056)
关键词 银杏内酯B 线粒体 活性氧 Ginkgolide B Mitochondria Reactive oxygen species
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参考文献15

  • 1Zhang C,Tian X,Luo Y,et al.Ginkgolide B attenuates ethanolinduced neurotoxicity through regulating NADPH oxidases[J].Toxicology,2011,287(1-3):124-130.
  • 2Vincent AM,Brownlee M,Russell JW.Oxidative stress and programmed cell death in diabetic neuropathy[J].Ann N Y Acad Sci,2002,959:368-383.
  • 3Maclennan KM,Darlington CL,Smith PF.The CNS effects of Ginkgo biloba extracts and ginkgolide B[J].Prog Neurobiol,2002,67(3):235-257.
  • 4Pop-Busui R,Sima A,Stevens M.Diabetic neuropathy and oxidative stress[J].Diabetes Metab Res Rev,2006,22(4):257-273.
  • 5Chan WH,Hsuuw YD.Dosage effects of ginkgolide B on ethanolinduced cell death in human hepatoma G2 cells[J].Ann N Y Acad Sci,2007,1095:388-398.
  • 6Allen DA,Harwood S,Varagunam M,et al.High glucose-induced oxidative stress causes apoptosis in proximal tubular epithelial cells and is mediated by multiple caspases[J].FASEB J,2003,17(8):908-910.
  • 7Srinivasan S,Stevens MJ,Sheng H,et al.Serum from patients with type 2 diabetes with neuropathy induces complementindependent,calcium-dependent apoptosis in cultured neuronal cells[J].J Clin Invest,1998,102(7):1454-1462.
  • 8Huang M,Qian Y,Guan T,et al.Different neuroprotective responses of Ginkgolide B and bilobalide,the two Ginkgo components,in ischemic rats with hyperglycemia[J].Eur J Pharmacol,2012,677(1-3):71-76.
  • 9Chance B,Sies H,Boveris A.Hydroperoxide metabolism in mammalian organs[J].Physiol Rev,1979,59(3):527-605.
  • 10Young TA,Cunningham CC,Bailey SM.Reactive oxygen species production by the mitochondrial respiratory chain in isolated rat hepatocytes and liver mitochondria:studies using myxothiazol[J].Arch Biochem Biophys,2002,405(1):65-72.

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