中文摘要：

目的 探讨中药复方脑络欣通及其拆方抗气虚血瘀证脑缺血再灌注损伤的作用机制。方法 复制大鼠气虚血瘀证模型，线栓法大脑中动脉制作局灶性脑缺血再灌注模型，随机分为假手术组、模型组、益气组、活血组和脑络欣通组，予相应处理；采用免疫组织化学染色SABC法检测额顶叶皮质缺血半暗带区GFAP、bFGF和GDNF蛋白表达。结果 模型组GFAP、bFGF和GDNF蛋白表达较假手术组明显增强（P〈0．01）；各治疗组与模型组比较，在脑缺血再灌注48h和72h均有显著差异（P〈0．05或0．01）；在脑缺血再灌注24h，部分治疗组与模型组有显著差异（P〈0．05）；各治疗组间在脑缺血再灌注48h或72h有显著差异（P〈0．05）。结论 脑络欣通可通过抑制GFAP的表达，促进bFGF和GDNF蛋白的表达，调节不同细胞间相互作用，改善气虚血瘀证脑缺血再灌注损伤。

英文摘要：

Objective： To investigate the mechanism of Naoluoxintong in improving on local cerebral ischemia and reperfusion effect. Methods： The local cerebral ischemia and reperfusion model was established by intraluminal thread occlusion of the middle cerebral arteries （MCAO） after qi - deficiency and blood stasise syndrome model was established by high lipid diet, hunger and swimming. The test animals were divided into sham group, model group, Yiqi group, Huoxue group and Naoluoxintong group. The expression of GFAP, bFGF and GDNF Protein were observed in ischemic penumbra of the cortex of frontal or pariedal lobe by immunohistochemical SABC staining. Results： The positive cell area of GFAP, bFGF and GDNF protein expression in model group were higher than those in sham group. The postive cell area of bFGF and GDNF in all treatment groups for 48h and 72h were higher than those in model group, GFAP was lower. The positive cell area of bFGF and GDNF in Huoxue and Naoluoxintong group for 24h were higher than those in model group. Therapeutic effect in Naoluoxintong group were superior to that in Yiqi and Huoxue group for 24 or 48 hours. Conclusion： Naoluoxintong can regulate inreaetion between neuron and neuroglial cells, alleviate pathologic injury after focal cerebral ischemia and reperfusion with qi deficiency and blood stasis in MCAO rats by promoting the expression of bFGF and GDNF protein and inhibiting the exepression of GFAP.