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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。
Objective To investigate the effect of edaravone on focal cerebral ischemia-reperfusion injury and its possible neuroprotective mechanism. Methods The rat model of focal cerebral ischemia-reperfusion injury was established by thread occlusion method. The content of malondialdehyde (MDA) and the activity of nitric oxide synthase (NOS) in the brain tissue were detected by kit. The brain water content Immunohistochemical staining was used to detect the expression of aquaporin 4 (AQP-4). Results After ischemia-reperfusion injury, MDA content and NOS activity in rat brain increased, MDA content and NOS synthase activity increased at 30 min after cerebral ischemia-reperfusion in 3d peaked and returned to normal after 7 days. The water content of brain tissue increased at 1 day after cerebral ischemia-reperfusion, peaked at 3 days and decreased to approximately normal level at 7 days. The expression of AQP-4 in cerebral ischemia- 6h after perfusion increased, peaked at 3d, and dropped to approximately normal level on the 7th day. Edaravone can significantly reduce the MDA content and NOS activity, reduce the water content of brain tissue, and significantly reduce the expression of AQP-4. Conclusion After cerebral ischemia-reperfusion injury, edaravone can reduce lipid peroxidation injury by eliminating free radicals and protect neurons against cerebral edema by inhibiting the expression of AQP-4.