中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (3): 268-275.doi: 10.4103/1673-5374.128220

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

阿托伐他汀保护脑缺血再灌注损伤的途径

  

  • 收稿日期:2013-11-02 出版日期:2014-02-15 发布日期:2014-02-15
  • 基金资助:

    湖南省自然科学基金(11JJ5081),湖南省科技厅科技计划项目(2012SK3226和2011SK3236)。

Atorvastatin protects against cerebral ischemia/reperfusion injury through anti-inflammatory and antioxidant effects

Qiuyun Tu1, Hui Cao2, Wei Zhong2, Binrong Ding1, Xiangqi Tang2   

  1. 1 Department of Geriatrics, Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China
    2 Department of Neurology, Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China
  • Received:2013-11-02 Online:2014-02-15 Published:2014-02-15
  • Contact: iangqi Tang, M.D., Department of Neurology, Second Xiangya Hospital of Central South University, Changsha 410000, Hunan Province, China, txq6633@126.com.
  • Supported by:

    This work was supported by the Natural Science Foundation of Hunan Province in China, No. 11JJ5081; grants from Hunan Provincial Science and Technology Department in China, No. 2012SK3226 and 2011SK3236; the National Natural Science Foudation of China, No. 81271298/H0906.

摘要:

阿托伐他汀除具有降脂作用外,尚有抗炎、抗氧自由基等多种独立于其降脂作用的效果。实验设想阿托伐他汀对脑缺血再灌注损伤组织可起到保护作用。鉴于此,采用阿托伐他汀6.5 mg/kg对大鼠灌胃干预1周,再建立大脑中动脉缺血再灌注大鼠模型。免疫组化染色及分光光度计法检测结果显示,缺血再灌注损伤后大鼠大脑皮质缺血区可出现炎症相关因子E-选择素和髓过氧化物酶表达上调,氧化应激相关因子丙二醛含量上调及过氧化物歧化酶活性下降,阿托伐他汀预处理大鼠可显著抑制此趋势。结果证实阿托伐他汀能通过抗炎及抗氧化的途径保护大鼠脑缺血再灌注损伤。

关键词: 神经再生, 脑损伤, 脑缺血再灌注, 阿托伐他汀, E-选择素, 髓过氧化物酶, 过氧化物歧化酶, 丙二醛, 炎症反应, 氧自由基, 血脑屏障, 脑卒中

Abstract:

In addition to its lipid-lowering effect, atorvastatin exerts anti-inflammatory and antioxidant effects as well. In this study, we hypothesized that atorvastatin could protect against cerebral ischemia/reperfusion injury. The middle cerebral artery ischemia/reperfusion model was established, and atorvastatin, 6.5 mg/kg, was administered by gavage. We found that, after cerebral ischemia/reperfusion injury, levels of the inflammation-related factors E-selectin and myeloperoxidase were upregulated, the oxidative stress-related marker malondialdehyde was increased, and superoxide dismutase activity was decreased in the ischemic cerebral cortex. Atorvastatin pretreatment significantly inhibited these changes. Our findings indicate that atorvastatin protects against cerebral ischemia/reperfusion injury through anti-inflammatory and antioxidant effects.

Key words: nerve regeneration, brain injury, cerebral ischemia/reperfusion, atorvastatin, E-selectin, myeloperoxidase, superoxide dismutase, malondialdehyde, inflammation, free radicals, blood-brain barrier, stroke, NSFC grant, neural regeneration