神经节苷脂GM．1对脑缺血再灌注大鼠诱导型．氧化氮合成酶的影响

Effect of gangliaside GM1 on induced nitric oxide synthase after focal cerebral ischemical reperfusion in rats

目的:研究单唾液酸四已糖神经节苷脂(GM-1)对脑缺血再灌注后诱导型一氧化氮合成酶(iNOS)的影响并探讨其可能机制。方法:采用线栓法制作大鼠大脑中动脉闭塞模型,缺血2h再灌注22h。将雄性SD大鼠随机分成假手术组,模型对照组和GM-1处理组(15、30、60mg/kg3个给药剂量组)。通过红四氮唑(TTC)染色和图像分析计算各组脑梗死体积,采用生物化学法测量各组伤侧脑中NO含量和iNOS活性。结果:与模型对照组相比,GM-1中、高剂量处理组脑梗死体积缩小,iNOS活性和NO量下降,低剂量组变化不明显。结论:脑缺血后iNOS升高与脑损伤关系密切,而GM-1可以对抗iNOS和NO上升,并减轻脑缺血损伤。

Objective：To study the effect of gangliaside GM-1 on induced nitric oxide synthase （iNOS） after cerebral ischemic reperfusion and approach its possible mechanism. Methods：Using 2 h ischemia and 22 h reperfusion middle cerebral artery occlusion model, male SD rats were randomly divided into sham-operated group,model control group and GM-1 treat group which received GM-1 at doses of 15,30 or 60 mg/kg. The infarct size was evaluated by 2,3,5-triphenyhetrazolium chloride （TI＇C） staining and image assay. The NO content and the activity of induced nitric oxide synthase（iNOS） were determined by biochemical assay. Results：In comparison with model control group,the infarct size,iNOS activity and NO content were decreased in the groups receiving GM-1 at both middle and high dose except low dose. Conclusion：The rise of iNOS activity could correlate closely with brain injury,and GM-1 could reduce iNOS activity, NO connect and brain injury after cerebral ischemia.