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Research Article

阿米洛利缓解短暂性全脑缺血并参与中枢IL-6和TNF-α信号后的神经功能缺损

卷 19, 期 8, 2019

页: [597 - 604] 页: 8

弟呕挨: 10.2174/1566524019666190704100444

价格: $65

摘要

背景：中枢促炎细胞因子（PIC）信号参与了由心脏骤停（CA）引起的短暂性整体缺血后的神经功能缺损。 本研究旨在检查在中枢神经系统中使用阿米洛利阻断酸敏感离子通道（ASICs）是否可以缓解诱发CA后的神经功能缺损，并进一步检查PIC信号参与海马对阿米洛利的影响。 方法：窒息诱导CA，然后进行大鼠心肺复苏。 Western blot分析和ELISA用于确定海马中ASIC亚基ASIC1的蛋白表达以及PICs的水平。 如上所述，尽管在本研究中将阿米洛利和其他药理药物注入大脑，但临床上不太可能使用此程序。 结果：与对照动物相比，CA增加了大鼠海马中的ASIC1。 这与IL-1β，IL-6和TNF-α以及Caspase-3和Caspase-9的增加有关。 阿米洛利向侧脑室的给药减弱了Caspase-3 / Caspase-9的上调，进一步减轻了神经系统的严重程度评分和脑水肿。 抑制中枢IL-6和TNF-α也降低了CA大鼠海马中的ASIC1。 结论：CA引起的短暂性全脑缺血可能通过PIC信号放大海马中的ASIC1a。 施用至中枢神经系统的阿米洛利在整体缺血的过程中起神经保护作用。 因此，建议针对ASIC（即ASIC1a）治疗和改善CA诱发的全脑缺血。

关键词: ASIC，阿米洛利，心脏骤停，心肺复苏，海马，整体缺血。

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