中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2012, Vol. 7 ›› Issue (11): 837-841.

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

Propofol inhibits inflammation and lipid peroxidation following cerebral ischemia/ reperfusion in rabbits

  

  • 收稿日期:2012-01-04 修回日期:2012-03-24 出版日期:2012-04-15 发布日期:2012-04-15

Propofol inhibits inflammation and lipid peroxidation following cerebral ischemia/ reperfusion in rabbits

Xiaodong Wei1, Xing Wan1, Bo Zhao1, Jiabao Hou1, Min Liu1, Bangchang Cheng2   

  1. 1  Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
    2  Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
  • Received:2012-01-04 Revised:2012-03-24 Online:2012-04-15 Published:2012-04-15
  • Contact: Bangchang Cheng, Ph.D., Professor, Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China wxdrm@yahoo.com.cn
  • About author:Xiaodong Wei☆, Ph.D., Associate chief physician, Department of Anesthesiolo-gy, Renmin Hospital of Wu-han University, Wuhan 430060, Hubei Province, China

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Abstract:

The present study established a rabbit model of global cerebral ischemia using the ‘six-vessel’ method, which was reperfused after 30 minutes of ischemia. Rabbits received intravenous injection of propofol at 5 mg/kg prior to ischemia and 20 mg/kg per hour after ischemia until samples were prepared. Results revealed that propofol inhibited serum interleukin-8, endothelin-1 and malondialdehyde increases and promoted plasma superoxide dismutase activity after cerebral ischemia/reperfusion. In addition, cerebral cortex edema was attenuated with little neuronal nuclear degeneration and pyknosis with propofol treatment. The cross-sectional area of neuronal nuclei was, however, increased following propofol treatment. These findings suggested that propofol could improve anti-oxidant activity and inhibit synthesis of inflammatory factors to exert a protective effect on cerebral ischemia/reperfusion injury.

Key words: ischemia/reperfusion injury, propofol, endothelin-1, interleukin-8, malondialdehyde, superoxide dismutase, neuroprotection