Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, PR China.
Neuroscience. 2011 May 19;182:177-83. doi: 10.1016/j.neuroscience.2011.01.017. Epub 2011 Jan 14.
Edaravone is currently being used in acute ischemic stroke both in clinical and experimental research as a potent antioxidant. Here we explore the effects of edaravone on delayed neuronal death (DND) and long-dated cognitive dysfunction of hippocampus after cerebral ischemia-reperfusion (IR) injury and explain the underlying mechanisms and pathways. Our findings suggested that edaravone not only significantly alleviated delayed neuronal death and cognitive dysfunction of hippocampus after cerebral focal ischemia, but also markedly decreased malondialdehyde (MDA) levels. In addition, edaravone increased superoxide dismutase (SOD) levels and reduced the levels of inflammatory cytokines such as IL-1β and TNF-α expression; edaravone, also suppressed glial fibrillary acidic protein (GFAP) proliferation at days 3, 7 and 30 after reperfusion. Overall, the consensus emerging from this body of data indicated that edaravone exerts a later neuroprotective effect to hippocampus through its ability to inhibit inflammation, suppression of astrocyte activation and scavenging free radicals in stroke events.
依达拉奉目前被应用于急性缺血性脑卒中的临床和实验研究中，作为一种有效的抗氧化剂。在这里，我们探讨了依达拉奉对脑缺血再灌注（IR）损伤后迟发性神经元死亡（DND）和海马长时程认知功能障碍的影响，并解释了其潜在的机制和途径。我们的研究结果表明，依达拉奉不仅显著减轻了脑局灶性缺血后海马的迟发性神经元死亡和认知功能障碍，而且还显著降低了丙二醛（MDA）的水平。此外，依达拉奉增加了超氧化物歧化酶（SOD）的水平，并降低了白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）等炎症细胞因子的表达水平；依达拉奉还抑制了再灌注后第 3、7 和 30 天的胶质纤维酸性蛋白（GFAP）的增殖。总的来说，这些数据表明，依达拉奉通过抑制炎症、抑制星形胶质细胞的激活和清除自由基，对脑卒中事件中的海马发挥了迟发性神经保护作用。
