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Effects of Edaravone on JNK signaling pathway and neuronal autophagy in the hippocampus in SAH rats
Author(s): 
Pages: 531-535
Year: Issue:  6
Journal: Journal of International Neurology and Neurosurgery

Keyword:  EdaravoneSubarachnoid hemorrhageAutophagyJNK signaling pathway;
Abstract: 目的 探讨依达拉奉对蛛网膜下腔出血大鼠JNK信号通路及海马区神经细胞自噬的影响.方法 雄性SD大鼠40只,随机等分为假手术组(Sham组)、SAH模型组、依达拉奉治疗组(Edaravone组)、JNK抑制剂组(SP600125组).改良血管内穿刺法制成大鼠SAH模型;SP600125组于建模前30min,侧脑室注射SP600125(3μg/μl,10μl);Edaravone组于建模后5 mg/kgEdaravone腹腔注射,12h后重复给药.24h处死,检测各组海马区神经元形态、数量及Beclin-1、LC3-Ⅱ、p-JNK蛋白的变化.结果 与Sham组相比,SAH组海马区神经元排列紊乱、细胞多呈三角锥形、存活数量明显减少,(P<0.05);Beclin-1、LC3-Ⅱ、p-JNK表达升高,(P<0.05).与SAH组相比,Edaravone组、SP600125组神经元坏死率明显下降、形态正常细胞数增多,(P<0.05);Beclin-1、LC3-Ⅱ、p-JNK表达明显降低,(P<0.05).结论 依达拉奉可降低SAH大鼠海马区神经元Beclin-1和LC3-Ⅱ表达,减轻SAH后早期脑损伤,其可能是JNK通路依赖性的.
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