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长托宁对癫痫持续状态大鼠海马神经元保护作用研究 被引量:2

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摘要 目的探讨长托宁干预对癫痫持续状态(SE)后大鼠海马神经元损伤的保护作用及其可能机制。方法54只Wistar大鼠随机分为A组(对照组)、B组(模型组)和C组(长托宁组),后两组又分为6h、12h、24h、48h亚组。应用氯化锂-匹罗卡品制备SE模型。TUNEL法检测大鼠海马细胞凋亡,免疫组化法检测Bcl-2和Caspase-3的表达。结果SE后6h海马组织可见TUNEL、Caspase-3和Bcl-2阳性细胞表达,TUNEL和Caspase-3表达高峰均在24h;Bcl-2表达高峰在12h。C组各时间点TUNEL、Caspase-3阳性细胞较B组减少(除6h外,均P<0.05),而Bcl-2阳性细胞数增加(除6h外,均P<0.05)。结论长托宁可以上调Bcl-2,下调Caspase-3,长托宁可能通过抑制SE后海马神经元凋亡的机制,减轻SE时脑组织损伤,起到脑保护作用。
出处 《中西医结合心脑血管病杂志》 2010年第3期329-330,共2页 Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
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