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.