大鼠脑缺血后缺血区VEGF表达变化及通心络的影响

目的观察大鼠脑缺血后缺血区VEGF mRNA及蛋白水平随时间表达的变化及通心络对其的影响。方法制备大鼠大脑中动脉梗塞局灶性脑缺血模型，采用RT—PCR法及免疫组化法检测脑缺血后每组实验动物不同时间缺血区VEGFmRNA及蛋白表达的变化以及通心络的作用。结果1、正常大鼠脑缺血后脑组织中VEGFmRNA表达很少，大鼠局灶性脑缺血后VEGF mRNA表达逐渐增强，3d达高峰，缺血7d后叉降至约正常水平。VEGF主要在神经元阳性表达，表达趋势与mRNA基本吻合。2、通心络高剂组VEGF mRNA表达显著增强（p〈0.01，p〈0.05）；通心络各组vEGF阳性神经元数量增加：结论局灶性脑缺血可促进缺血区内源性神经保护因子VEGF高表达；通心络可增强和延长缺血区VEGF高表达，发挥对脑缺血的保护作用.

The VEGF expression of brain tissue in rats subjected with focal cerebral ischemia and the effects of TXL on this change.

To investigate the change of VEGF mRNA and protein expression after focal cerebral ischemia and the effects of Tongxinluo(TXL) on it. Methods The focal cerebral ischemic injury in rats was induced with inserting nylon thread into the onset of middle cerebral artery. The rats were divided into four groups randomly according to the post-surgery time: 3h, 24h, 3d and 7d. And each group was divided into four sub-groups: the sham group,the model group, TXL high-dose (2.24 chain reaction (RT-PCR) and the immunohistochemical staining were used to determine the expression of VEGF. Results 1.The VEGF expression of brain tissue in rats subjected with focal cerebral ischemia :The mRNA expression of VEGF was slightly positive in sham group and its expression increased gradually in ischemic area at 3h, 24h and 3d after focal ischemia. The expression reached the peak at 3d and recovered to the normal level again at 7d. Histochemical staining results were described as below: The expression of VEGF is slightly positive in sham group.Positive plasma brown stain in neurocytes, gliocytes and endothelium in ischemic brain tissue were detected.And the stain was intensified gradually from 3h to 72h.2. The effects of TXL on the VEGF expression of brain tissue in rats subjected with focal cerebral ischemia:Compared with model group, the mean expression level of VEGF mRNA in TXL high-dose group (2.24g/ kg) at 3h and 24h presented augmentative tendency, but there is no significant difference between these groups due to the extensive standard deviation intergroup. At 3d after focal ischemia ,the VEGF mRNA expression increased remarkably(P<0.01).The dose could prolong the expression time of VEGF mRNA, namely at 7d its expression remained high level.And compared with model group, the expression level increased obviously(P<0.05). Histochemical staining results show that: AT each time point after focal ischemia,the positive neuron amounts increased in TXL groups. Conclusions The expression of VEGF after focal brain ischemia, an endogenous neuroprotective factor, was promoted to facilitate the neuron injury recovery. TXL could increase and prolong the the expression level of VEGF, this may be favorable to the focal cerebral injury recovery.