人参总皂甙对大鼠脑缺血的保护机制的研究

The investigation on protective mechanism of SPG to the focal cerebral ischemia in rats

目的:探讨人参总皂甙(SPG)对大鼠局灶性脑缺血的保护作用及其机制。方法:用线栓法制成大鼠大脑中动脉闭塞(MCAO)模型,放射性同位素法测定脑微血管及脑组织中一氧化氮合酶(NOS)活性,用红四氮唑(TTC)染色、图像分析仪测定梗塞体积,显微镜观察病理变化。结果:局灶性脑缺血大鼠不同部位、不同时相的NOS活性不同,脑微血管中NOS活性在缺血4h(I4)组明显升高(P<0.01),脑组织(纹状体,海马)的NOS活性在I4却明显降低(P<0.01,P<0.05),同时梗塞体积扩大、病理改变明显加重。SPG使缺血4h(I4G)组脑微血管中NOS活性明显低于脑缺血4h(I4)组(P<0.01),而脑组织(纹状体、海马)NOS活性明显高于I4组(P<0.05,P<0.01),并伴随梗塞体积的减小(P<0.01)及病理变化的减轻。结论:脑微血管中NOS活性变化在局灶性脑缺血损伤中起重要作用,脑组织中NOS活性变化也参与了其病理生理过程。SPG对MCAO大鼠有明显的保护作用,其机制可能是通过降低脑微血管中NOS活性及使脑组织中的NOS活性维持在一定水平上而实现的。

Obiective:To investigate the protective role of the traditional Chinese medicine saponions of panax ginseng(SPG)to the brain of rat middle cerebral artery occlusion(MCAO)model and its mechanism.Methods:The NOS ativity in the cerebral microvessels and tissues was determined by radioisotopic method.Infarct volume was measured by TTC staining and imagic analysis.Pathological changes were observed by HE stained sections.Results:The NOS activity of ischemia 4 hours(I4) in the cerebral microvessels was obviously higher than that of the sham group(P<0.01),but the activity of NOS activity in the cerebral tissues (striatum,hippocampus) decreased more than that of the sham group (P<0.01,P<0.05).Meanwhile,the enlargement of infarct volume and the remarkable changes of pathology were also found.The NOS activity in the cerebral microvessels of SPG ischemia 4 hours(I4G) group was obviously lower than that of I4 group(P<0.01),but the NOS activity in cerebral tissues (striatum,hippocampus )of I4G group was higher than that of I4 group (P<0.05,P<0.01).Meanwhile companied with the decrease of infarct volume and less ischemic injury of pathology than that of I4 group.Conclusion:NOS activity in the cerebral microvessels played an important role during the cerebral injury of focal cerebral ischemia,and the NOS activity in the cerebral tissues contributed some role,too.SPG played remarkable protective effect on the brain of MCAO rat model,the mechanism could be through inhibiting the increase of NOS activity in the cerebral microvessels and in the meantime maintaining NOS activity in cerebral tissues at a certain level .