| Objective: In this study , we observed the apoptosis and its relation to the expression of TGF-β1 and Caspase-3 after focal cerebral ischemia and reperfusion in rats, investigated pathologic mechanism after cerebral ischemia.Methods: Stroke-prone renovascular hypertensive (RHRSP) rats were selected, the middle cerebral artery occlusion and reperfusion (MCAO/R) was established by inserting nylon thread coated with paraffin . The 42 Stroke-prone renovascular hypertensive rats were randomly divided into seven groups: sham-operated group, simple ischemia 2-hour(2h), ischemia 2h and reperfused 3h,6h,24h,48h,72h after the middle cerebral artery occlusion, After the MCAO was made, each of the group was divided into two groups. group 1: Immunocytochemistryt was performed to determine the level of TGF-β1 and Caspase-3. group 2 : the apoptosis of neurons were observed by flow cytometry.Results: 1. MCAO/R established by inserting nylon thread coated with paraffin is a good ischemia and reperfusion model. 2.The sham group showed a few apoptotic cells. The number of apoptotic cells increased with the development of reperfusion, and reached its the highest level at 48h,then the number of apoptotic cells decreased at 72h. 3. The expression of TGF-β1 and Caspase-3 was predominantantly upregulated in the perinfarct region, the expression of TGF-β1 increased faster, peaking at 24h of reperfusion; the expression of Caspase-3 increased slower, peaking at 48h of reperfusion.Conclusion: 1. the number of apoptotic cells is changing after focal cerebral ischemia and reperfusion in rats, and apoptosis is an important way of neuron death; 2.The expression of TGF-β1 and Caspase-3 are upgraded in ischemical reperfusion injury. Peaking time of TGF-β1 is earlier than Peaking time of Caspase-3 ,which suggest TGF-β1 play an important role in the mechanism of apoptosis by regulating Caspase-3.
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