The Effects Of Yindanxinnaotong Preconditioning On Neural Cell Apoptosis In Rats With Cerebral Ischemia Reperfusion

Objective:To investigate the effects of Yindanxinnaotong (YDXNT) preconditioning on neural cell apoptosis, B-cell lymphoma-2(Bcl-2) and asparagic acid specific cysteine protease-3(Caspase-3) expression in cerebral ischemia-reperfusion rats, and explore the mechanisms of YDXNT treatment for cerebrovascular disease.Methods:Thirty-two male SD rats were randomly divided into sham-operated group, model group, Nimodipine group and YDXNT group. Continuous intragastric administration for7ds once a day, sham operated group and model group were given isovolumic distilled water. Middle cerebral occlusion (MCAO) of rat was caused by suture according to Longa etal in eighth day, and brain tissue was extracted after reperfusion24hours. The infarct area was evaluated by weight percent, positive cells of neural cell apoptosis was measured by TUNEL marked, and the level of Caspase-3and Bcl-2expression were measured by immunohistochemical methods. To approach the protective effects and mechanism of YDXNT preconditioning in focal cerebral ischemia reperfusion rats through the analysis of variability.Results:The neurological deficits score was significantly increased in ischemia-reperfusion groups compared with the sham operated group, occurred obvious infarct area, neural cell apoptosis and Caspase3expression were decreased, and Bcl-2expression was increased (P<0.05); infarct area, neural cell apoptosis and Caspase-3expression were decreased, Bcl-2expression was increased in Nimodipine group and YDXNT group comparing with model group (P<0.05), but no neurological deficits score(P>0.05). There was no difference between Nimodipine group and YDXNT group (P<0.05), except Bcl-2(P<0.01).Conclusion:YDXNT has protective effect on focal cerebral ischemia-reperfusion injury, can decrease neural cell apoptosis, the mechanism may be related to increasing Bcl-2expression, decreasing Caspase-3expression.