脑缺血-再灌注损伤模型MMP9、Bcl-2的表达及黄酮的干预作用

目的 探讨MMP9、Bcl-2在脑缺血损伤中的作用以及黄酮对脑缺血损伤保护作用机制。方法 应用免疫组化技术观察MMP9、Bcl-2蛋白表达。结果 模型组缺血再灌注20min后CAI区的MMP9表达明显增加，其阳性细胞数与假手术组对比有明显差异，黄酮可使其表达显著降低；黄酮组与脑缺血再灌注组相比Bcl-2阳性细胞数显著增多。结论 脑缺血再灌注可诱导海马CM区的MMP9表达增加，MMP9表达增加可能是脑缺血再灌注损伤的机制之一；黄酮可抑制MMP9表达，提高Bcl-2蛋白表达，从而对脑缺血再灌注损伤具有保护作用。

The study of MMP9, Bcl-2 expression after brain ischemia reperfusion and the treatment of flavone

Objective To explore the role of MMP9, Bcl-2 during cerebral ischemia reperfusion and the mechnism of the flavone neuroprotective effect on the brain injury induced by cerebral ischemia-reperfusion.Methods Immunohistochemistry was used to measure the protein expression of MMP9 after cerebral ischemia and reperfusion.Result MMP9 expression was significantly increased after ischemia reperfusion in CA1 in model group ,compared with sham-operated group,P<0.05.In flavone group,the MMP9 expression was lower than that in model group,P<0.05. Bcl-2 positive cell number of ischemic sides in flavone group was higher than that in model group. Conclusion These results demonstrate the increase MMP9 expression in CA1 induced by cerebral ischemia reperfusion and MMP9 may be one of the molecular mechanisms of brain damage;flavone were of the neuroprotective effect on the brain injury induced by cerebral ischemia and reperfusion by regulating MMP9 and Bcl-2.