[Abstact] Objective To explore the protective effects of the Baimai ( BM ) therapy on focal cerebral ischemia-reperfusion injury in rats and the influence of BM therapy on Jagged1 expression of hipp-ocampal dentate gyrus. Methods The focal cerebral ischemia-reperfusion injury models were induced by suture method, inserting thread 1. 5 h and reperfusion 7 d and 14 d respectively. The rats were randomly divided into sham-operation group, model group, Baimai therapy group ( BMT group) . The area of cerebral infarction was observed by TTC staining, the morphological changes of cortex cell was observed by HE staining, and immunohistochemistry method was used to detect hippocampal dentate gyrus Jagged1 positive cell number of each group rats. Results (1) the TTC staining result showed that normal brain tissue was bright red, infarction area of the brain was pale, and with the prolongation of reperfusion time, the infarct area was enlarged. The areas of cerebral infarction of BMT group were less than model group, and there was a significant difference compared with model group on 14 days (P<0. 05). (2) HE staining showed that degree of injury of cortical neurons in the cerebral ischemia group was lower than that in the model group. (3) BM therapy can increase hippocampal dentate gyrus Jagged1 expression of cerebral ischemia rats, Jagged1 positive cells was higher than model group and control group, the result had significant difference (P<0. 05), after having operation 7 days and 14 days. Conclusions BM therapy has certain protective effect on focal cerebral ischemia-reperfusion injury, and can promote Jagged1 expression in hipp-ocampal dentate gyrus after rats having focal cerebral ischemia-reperfusion injury, the increase of Jagged1 expression may be one of the molecular mechanisms of the proliferation and differentiation of endogenous neural stem cells after cerebral ischemia injury via the Notch pathway.%目的：探讨白脉疗法对局灶性脑缺血再灌注大鼠脑损伤的保护作用及对海马齿状回Jagged1表达的影响。方法线栓法制作局灶性脑缺血再灌注大鼠模型。随机分为假手术组、模型组、白脉疗法组,脑缺血1.5小时,分别再灌注7天、14天,通过氯化三苯基四氮唑( triphenyltetrazolium chloride,TTC)染色观察脑梗死面积,苏木精-伊红染色法( hematoxylin-eosin staining ,HE)染色观察皮层细胞形态变化,并应用免疫组化法检测各组大鼠海马齿状回Jagged1阳性细胞数量。结果(1) TTC染色观察到正常脑组织呈鲜红色,梗死区脑组织呈苍白色,并且随着再灌注时间的延长可见梗死区扩大,白脉疗法组的脑梗死体积小于模型组,且14天时与模型组比较有显著性差异(P<0.05)。(2) HE染色表明白脉疗法组脑缺血大鼠皮层神经元的损伤程度低于模型组。(3)白脉疗法可以上调脑缺血大鼠海马齿状回SGZ的Jagged1表达,术后7天、14天Jagged1阳性细胞数高于模型组、假手术组,且有显著性差异(P<0.05)。结论白脉疗法对局灶性脑缺血再灌注大鼠脑损伤有一定的保护作用,且可促进大鼠局灶性脑缺血再灌注损伤后海马齿状回区Jagged1的表达,Jagged1的表达增加可能是白脉疗法通过Notch通路促进脑缺血损伤后内源性神经干细胞增殖分化的分子机制之一。
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