Objective: we observed the apoptosis and the expression of IGF-â… and Bcl-2 after cerebral ischemia and reperfusion in hypertensive and no hypertension rats in order to investigate the mechanism of hypertensive cerebral ischemical reperfusion injury.Methods: Stroke-prone renovascular hypertensive (RHRSP) rats and no hypertension rats were selected and the middle cerebral artery occlusion and reperfusion (MCAO/R) was established by inserting nylon thread coated with paraffin.The 24 RHRSP rats and the 24 no hypertension rats were randomly divided into cerebral ischemia 2h and reperfusion 3h,6h,24h,48h,respectively.Each group have six rats.Brain tissue was taken after the MCAO/R.Immunocytochemistryt was performed to determine the level of IGF-â… and Bcl-2.The apoptosis were observed by flow cytometry.Hematoxylin eosin(HE) staining was observed.Results: 1.Compared with no hypertension rats,the apoptosis obviously increased in hypertensive rats(p<0.05,or p<0.01).This increasing was continuing from cerebral ischemia 2h and reperfusion 3h to cerebral ischemia 2h and reperfusion 48h.2. Compared with no hypertension rats,the expression of IGF-â… and Bcl-2 was down regulated(p<0.05,or p<0.01).This changing was continuing.Conclusion: 1. The apoptosis increasing was a cause of hypertension aggratating cerebral ischemical reperfusion injury.2.The expression of IGF-â… and Bcl-2 decreasing was problem a mechanism of hypertension aggratating cerebral ischemical reperfusion injury.
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