上海交通大学学报（医学版）

上海交通大学学报（医学版）

• 论著（基础研究） • 上一篇    下一篇

尿酸对氧糖剥夺/再灌注损伤的PC12细胞的保护作用

刘 宣1，王海嵘1，刘佳福1，陈向军2，卢孔渺1，潘曙明1   

  1. 1.上海交通大学  医学院附属新华医院急救中心， 上海 200092； 2.复旦大学附属华山医院神经内科， 上海 200040
  • 出版日期:2013-10-28 发布日期:2013-10-31
  • 作者简介:刘 宣（1988—）， 女， 硕士生; 电子信箱: shliuxuan@gmail.com。
  • 基金资助:

    上海市公共卫生人才培养计划(GWDTR201219)

Uric acid protects PC12 cells against oxygen-glucose deprivation/reperfusion-induced injury

LIU Xuan1, WANG Hai-rong1, LIU Jia-fu1, CHEN Xiang-jun2, LU Kong-miao1, PAN Shu-ming1   

  1. 1.Department of Emergency, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China; 2.Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China
  • Online:2013-10-28 Published:2013-10-31
  • Supported by:

    Shanghai Public Health Talents Cultivation Program, GWDTR201219

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摘要：

目的 探讨尿酸对氧糖剥夺/再灌注（OGD/R）损伤的PC12细胞的保护作用及其机制。方法 体外培养大鼠肾上腺嗜铬细胞瘤PC12细胞，根据对细胞处理方式的不同分为对照组、尿酸组、OGD/R组及OGD/R+尿酸组。以改良的噻唑蓝法（MTT）测定细胞活性，采用Annexin V-FITC/PI双染法检测细胞凋亡率，双氢罗丹明（DHR）检测细胞内活性氧簇（ROS）的水平，罗丹明123检测线粒体膜电位。结果 与对照组比较，OGD/R组PC12细胞活力显著降低，差异有统计学意义（P<0.05）；而在OGD/R的同时给予50~400 μmol/L尿酸处理，可以明显提高细胞活力。流式细胞仪检测结果发现，400 μmol/L尿酸可以显著减少OGD/R引起的细胞凋亡，抑制细胞内ROS产生和降低线粒体膜电位，与OGD/R组比较差异均有统计学意义（P<0.05）。结论 尿酸可以通过抑制ROS的产生稳定线粒体功能，从而发挥其对抗OGD/R损伤的神经保护作用。

关键词: 尿酸, PC12细胞, 氧糖剥夺/再灌注, 细胞凋亡, 活性氧簇生成, 线粒体膜电位

Abstract:

Objective To investigate the protective effect of uric acid on PC12 cells injured by oxygen-glucose deprivation/reperfusion (OGD/R), and explore the mechanism. Methods Rat PC12 cells cultured in vitro were divided into control group, uric acid group, OGD/R group and OGD/R+uric acid group based on different ways of treatment. The cell viability was assessed by the modified MTT method, Annexin V-FITC/PI double staining was employed to determine the apoptosis rate, dihydrorhodamine (DHR) was applied to measure the cellular reactive oxygen species (ROS) levels, and rhodamine 123(Rh123) was used to detect the mitochondrial transmembrane potential (ΔΨm). Results The viability of PC12 cells in OGD/R group was significantly lower than that in control group (P<0.05), while management with uric acid (50-400 μmol/L) during OGD/R significantly increased the cell viability. Flow cytometry revealed that 400 μmol/L uric acid significantly inhibited OGD/R-induced apoptosis, reduced intracellular ROS production and decreased mitochondrial transmembrane potential, which were significantly different from those in OGD/R group (P<0.05). Conclusion Uric acid may have a neuroprotective effect against OGD/R-induced injury by attenuating ROS production and preserving mitochondrial function.

Key words: uric acid, PC12 cells, oxygen-glucose deprivation/reperfusion, apoptosis, reactive oxygen species generation, mitochondrial transmembrane potential