益气活血通脉颗粒调控小胶质细胞介导脑缺血再灌注损伤的作用机制

The mechanism of Yiqi Huoxue Tongmai granule in regulating microglia to mediate cerebral ischemia-reperfusion injury

目的探讨益气活血通脉颗粒通过调控小胶质细胞介导脑缺血再灌注损伤的作用机制.方法采用BV2小胶质细胞(BV2)氧糖剥夺/复氧(OGDR)模型,实验共分为4组,空白组、OGDR模型组、空白血清组、含药血清组.除空白组外,其余三组均置于氧糖剥夺罐进行氧糖剥夺/复氧实验.取各组细胞上清液,应用ELISA试剂盒检测各组细胞中活性氧自由基(ROS)、白介素1β(IL-1β)和白介素18(IL-18)水平变化.结果与空白组比较,OGDR模型组与空白血清组小胶质细胞中ROS水平升高(P<0.01),与空白血清组比较,含药血清组小胶质细胞中ROS水平降低(P<0.05).与空白组比较,OGDR模型组与空白血清组小胶质细胞中IL-1β和IL-18水平升高(P<0.01),与空白血清组比较,含药血清组小胶质细胞中IL-1β和IL-18水平降低(P<0.01).结论益气活血通脉颗粒能降低ROS及IL-1β、IL-18水平,可以减弱缺氧复氧导致的小胶质细胞氧化应激反应及抵抗缺氧复氧导致的小胶质细胞炎性反应.

Objective To investigate the mechanism of Yiqi Huoxue Tongmai granule in regulaing microgia to mediate cerebral ischemia-reperfusion injury.Methods BV2 microgia(BV2)model of oxygen and sugar deprivation/reoxygenation(OGDR)were adopted.The experiment was divided into 4 groups:blank group,OGDR model group,blank serum group and Yiqi Huoxue Tongmai granules drug-contining serum intervention group.Except the blank group,the other three groups were placed in oxygen and sugar deprivaion tank for oxygen and sugar deprivation/reoxygenation experiment.The contents of reactive oxygen species(ROS),interleukin-1β(IL-1β)and interleukin-18(IL-18)in the supematant of each group were detected by ELISA kit.Results Compared with blank group,ROS content in microglia of OGDR model group and blank serum group was significantly increased(P<0.01).ROS content in microgia in drug-contaning serum group was signifcanly decreased compared with that in blank serum group(P<0.05).Compared with blank group,the contents ofIL-Iβand IL-18 in microglia of OGDR model group and blank serum group were extremely significanly increased(P<0.01),and the contents ofIL-Iβand IL 18 in drug containing serum group were extremely significandly decreased compared with blank serum group(P<0.01).Conclusion Yiqi Huoxue Tongmai granules can significantly reduce the content of ROS and the contents of inflammatory factors IL-1βand IL-18,indicating that Yiqi Huoxue Tongmai granules can reduce the oxidative stres response of microglia induced by hypoxia and reoxygenation and resist the infammatory response of microglia induced by hypoxia and reoxygenation.