抗凋亡基因bcl-2对大鼠脑梗死早期缺血部位基质金属蛋白酶-9的影响

The early effects of injection of pLXSN-bcl-2 cDNA on MMP-9 expression in ischemic focus of cerebral infarction rats

目的研究质粒pLXSN介导的bcl-2 cDNA对在大鼠脑梗死后缺血部位基质金属蛋白酶-9表达的影响,并探讨其可能存在的调节机制。方法60只成年雄性Wistar大鼠按随机原则分为2组:生理盐水组(n=30)和bcl-2组(n=30),每组再按照缺血再灌注后24、48、72h分为3个亚组。各组大鼠均成功制备MCAO模型,2h后再灌注;再灌注3h,经颈内动脉分别缓慢注射生理盐水及质粒pLXSN介导的bcl-2 cDNA 120μl。干湿重法测脑水含量;免疫组化法测定基质金属蛋白酶-9表达。结果与对照组相比,bcl-2组脑组织水肿明显减轻,基质金属蛋白酶-9阳性细胞数在相应时间点均有明显减少(P<0.05),两组基质金属蛋白酶-9蛋白表达均于再灌注48h左右达到高峰。结论在脑梗死数小时内,经颈内动脉注射质粒pLXSN介导的bcl-2 cDNA可以减轻对脑梗死后缺血区域的基质金属蛋白酶-9表达调节作用,降低基质金属蛋白酶-9的水平,并减轻脑水肿。

Objective To explore the early effects of pLXSN conducted bcl-2 gene on MMP-9 expression in ischemic focus of cerebral infarction of rats. Methods 60 adult male Wistar rats were assigned randomly to physiological saline group （n = 30） and pLXSN bcl-2 group （n = 30）. Each group was derided into 3 subgroups ：24h ,48h and 72h subgroup according to the time after reperfusion onset. Thereafter,middle cerebral artery occlusion （MCAO） was performed. Two hours after the occlusion, reperfusion was implemented. Then three hours later, Phy. saline and pLXSN bcl- 2 cDNA were injected slowly and respectively into internal carotid artery. Immunohistoehemistry method was used to detect MMP-9 expression . Results In experimental group, the water content of brain and MMP-9 expression decreased obviously compared with that of control groups（P 〈 0.05）. Conclusion In few hours after brain infarction, injection of pLXSN-bcl-2 cDNA can lower the MMP-9 expression level, decrease the reperfusion damage by MMP-9 and relieve brain edema.