N-乙酰半胱氨酸预防大鼠脑缺血/再灌注损伤的实验研究

The protective effect of N-acetyl cysteine on brain ischemia-reperfusion injury in rats

目的:研究在大鼠局灶性脑缺血模型中,N-乙酰半胱氨酸(NAC)预防脑组织的缺血/再灌注损伤的效果。方法:将30只体重220～250g的雄性Wister大鼠随机分成3组,假手术组、缺血再灌注组和NAC预处理组,Zea-Longa线栓法阻塞大脑中动脉(MCA)导致局灶性脑缺血45min,再灌注后24h后,对大鼠的神经功能缺失进行评分,TTC法评估脑梗死体积,bcl-2、Bax、TNF-α、iNOS免疫组化染色。结果:与非NAC处理组大鼠相比,NAC处理组大鼠脑梗死体积减少49.7%(P<0.01),神经学评分减少50%(P<0.01)TNF-α、Bax和iNOS的表达也明显减少(P<0.05),bcl-2的表达明显增加(P<0.05)。结论:NAC能通过抑制TNF-α、Bax和iNOS的表达、增加bcl-2的表达防治脑缺血和再灌注损伤。

Objective：To study the protective effect and mechanism of N-acetyl cysteine（NAC） on the middle cerebral ischemic-reperfusion injury（CIRI） in rats. Methods, The models of reperfusion twenty-four hours after forty-five minutes ischemia were established by Zea-Longa. Thirty male rats were divided randomly into sham operation group, the ischemia-reperfuaion group and NAC group. The neurological deficit scores were evaluated, the volume of brain infarction was measured with TTC, the expression of iNOS/bcl-2/Bax/TNF-a were tested with immunohistochemistry in brain tissue in rats Results：The infarction volume and the score of nerve function were significantly reduced in NAC group than those of the ischemia-reperfusion group（49.7% ,50% respectively）（both P〈0.01 ）, the expression of iNOS/TNF-a/Bax were reduced significantly, and bcl-2 increased significantly （P 〈 0. 05）. Conclusion NAC may protect the CIRI in rats by reducing the expression of iNOS/TNF-a/Bax and increasing expression of bcl-2.