依达拉奉对脑缺血-再灌注大鼠的神经保护作用及其机制研究

目的探讨依达拉奉对局灶性脑缺血-再灌注损伤的影响及其可能的神经保护机制。方法用线栓法制备大鼠局灶性脑缺血-再灌注损伤模型,用试剂盒检测脑组织丙二醛(MDA)含量和一氧化氮合酶(NOS)活性;分别测定脑组织含水量;免疫组织化学染色检测水通道蛋白4(AQP-4)的表达水平。结果缺血再灌注损伤后,大鼠脑组织脂质过氧化产物丙二醛含量和一氧化氮合酶活性增高,MDA含量和NOS合酶活性于脑缺血-再灌注后30min开始增高,于3d达到高峰,于7d基本恢复正常;脑组织含水量于脑缺血再灌注后1d开始增高,于3d达到高峰,于7d时下降至大致正常水平;AQP-4的表达于脑缺血-再灌注后6h开始增高,于3d达到高峰,于7d时下降至大致正常水平。依达拉奉干预能显著降低MDA含量和NOS活性,降低脑组织的含水量,并使AQP-4的表达明显下降。结论在脑缺血-再灌注损伤后,依达拉奉能通过清除自由基而减轻脂质过氧化损伤,并通过抑制AQP-4的表达减轻脑水肿,从而起到神经保护作用。

Mechanism and neuroprotective effect of edaravone on rats with focal cerebral ischemic-reperfussion model

Objective To investigate the neuroprotective mechanism and effect of Edaravone on focal cerebral ischemia-reperfusion injury.Methods Focal cerebral ischemia-reperfusion injury rats model was induced by reversible middle cerebral artery occlusion.Content of Malondialdehyde(MDA) and activity of NOS were measured by assay kits.To weight the water content in rat brain at each time point.Immunohistochemistry technology was used to test the expression of AQP-4.Results In MCAO / R group: the content of MDA and activity of NOS increased at 30 min,reached to maximum at 3 d and decreased to normal at 7 d;the brain water content increased at 1 d,reached to maximum at 3 d and decreased to normal at 7 d;the expression of AQP-4 gradually increased at 6 h,reached its peak at 3 d,and back to normal at 7 d,compared with control group.Compare with MCAO / R group,the MDA contents were much lower at 30 min,the NOS activities were significantly lower at 30 min and brain water contents were clearly lower at 1 d,3 d,7 d in Edaravone group.The expression of AQP-4 significantly decreased at 1 d,3 d,7 d in Edaravone group.Conclusions Edaravone has neuroprotective effects on ischemia / reperfusion injury rats by reducing MDA content and NOS activity,decreasing the expression of AQP-4 and inhibiting brain edema.