Article Summary
刘宣1 王海嵘1 刘佳福1 陈向军2 卢孔渺1 潘曙明1△.白藜芦醇对氧糖剥夺/ 再灌注损伤的PC12细胞的保护作用 及其作用机制*[J].现代生物医学进展英文版,2014,14(8):1423-1427.
白藜芦醇对氧糖剥夺/ 再灌注损伤的PC12细胞的保护作用 及其作用机制*
Protective Effect of Resveratrol on the Injury of PC12 Cells Induced byOGD/R and Its Mechanisms*
  
DOI:
中文关键词: 白藜芦醇  氧糖剥夺/再灌注  细胞凋亡  ROS 生成  SIRT1
英文关键词: Resveratrol  OGD/R  Apoptosis  ROS generation  SIRT1
基金项目:上海市公共卫生人才培养计划(GWDTR201219)
Author NameAffiliation
LIU Xuan, WANG Hai-rong, LIU Jia-fu,CHEN Xiang-jun, LU Kong-miao,PAN Shu-ming 1 上海交通大学医学院附属新华医院急救中心上海2000922 复旦大学医学院附属华山医院神经内科上海200040 
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中文摘要:
      摘要目的:探讨白藜芦醇对氧糖剥夺/再灌注(OGD/R)损伤的PC12 细胞的保护作用及其机制。方法:体外培养PC12 细胞,分为 对照组,白藜芦醇组,OGD/R 组及OGD/R+ 白藜芦醇组。以改良的噻唑蓝法测定细胞活性,采用Annexin V-FITC/PI 双染法检测 细胞的凋亡率,用双氢罗丹明(DHR)检测细胞内活性氧簇(ROS)的水平,采用蛋白印迹法(western blot)分析SIRT1 的蛋白表达情 况。结果:与对照组相比,经过OGD/R 损伤后,细胞活力显著降低。而在OGD/R 的同时给予10 μmol/L的白藜芦醇处理,可以明 显提高细胞活力。流式细胞仪检测发现,10 μmol/L 的白藜芦醇可以显著地减少OGD/R 引起的细胞凋亡,抑制细胞内的ROS 产 生。western blot 的结果提示,与对照组比较,白藜芦醇可提高SIRT1 的蛋白表达水平。结论:白藜芦醇可以通过抑制ROS 的产生 和上调SIRT1的表达等机制而发挥其对抗氧糖剥夺/再灌注损伤的神经保护性作用。
英文摘要:
      ABSTRACT Objective:To investigate the protective effect of resveratrol (RSV) on the injury of PC12 cells induced by oxygen glucose deprivation /reperfusion (OGD/R) and its mechanisms.Methods: PC12 cells cultured in vitro were divided into control group, RSV group, OGD/R group and OGD/R+RSV group. The cell viability was assessed by the modified MTT method. Annexin V-FITC/PI double staining was used to detect apoptosis rate. DHR123 was used to measure cellular ROS levels. Western blot was used to study the expression level of SIRT1.Results: Compared to the normal control group, the cell viability decreased significantly after OGD/R and giving 10 μmol/L RSV during OGD/R could significantly increase cell viability. Based on the results of flow cytometry, we found 10 μmol/L RSV markedly inhibited OGD /R-induced apoptosis and reduced intracellular ROS generation. Result of Western blot showed that RSV could increase the expression of SIRT1 compared with control group. Conclusion:RSV was found to have a neuroprotective effect against OGD/R-induced injury by attenuating ROS production and up-regulating the expression level of SIRT1.
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