Propofol inhibits inflammation and lipid peroxidation following cerebral ischemia/reperfusion in rabbits.
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.
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Xiaodong
X
Wei
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Xing
X
Wan
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Bo
B
Zhao
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Jiabao
J
Hou
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Min
M
Liu
Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
Bangchang
B
Cheng
endothelin-1; interleukin-8; ischemia/reperfusion injury; malondialdehyde; neuroprotection; propofol; superoxide dismutase