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首页> 外文期刊>Biochemistry and Cell Biology >Ectopic expression of Miro 1 ameliorates seizures and inhibits hippocampal neurodegeneration in a mouse model of pilocarpine epilepsy
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Ectopic expression of Miro 1 ameliorates seizures and inhibits hippocampal neurodegeneration in a mouse model of pilocarpine epilepsy

机译：Miro 1的异位表达改善癫痫发作并抑制柳甘蓝癫痫小鼠模型中的海马神经变性

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摘要

Epilepsy is a common disease of the central nervous system. This study aimed to investigate the role of mitochondrial Rho (Miro) 1 in epilepsy, using a mouse model of pilocarpine-induced status epilepticus (SE). Intraperitoneal injection of pilocarpine induced epileptic seizures in mice and significantly decreased Miro 1 expression in the hippocampus. Moreover, pilocarpine treatment increased the serum levels of heat shock protein 70 (HSP70) and S100 calcium binding protein B (S100B) and led to hippocampal neuronal injury and apoptosis. The intrinsic apoptotic pathway was activated in the hippocampal neurons following pilocarpine-induced SE, as evidenced by increased levels of cleaved caspase-3 and Bax, downregulation of Bcl-2, and the release of cytochrome c from mitochondria to cytoplasm. By contrast, forced expression of Miro 1 by lateral ventricular administration of adenovirus mitigated pilocarpine-induced epileptic seizures, reduced the elevation of HSP70 and S100B, and inhibited hippocampal neuronal apoptosis by suppressing the intrinsic apoptotic pathway. In summary, our data demonstrates that ectopic expression of Miro 1 alleviated pilocarpine-induced SE and protected hippocampal neurons by inhibiting the intrinsic apoptotic pathway. These findings provide new insights into epileptic disorders and suggest a potential neuroprotective value of Miro 1 in the treatment of epilepsy.
机译：癫痫是中枢神经系统的常见疾病。本研究旨在使用小鼠诱导的地位癫痫患者（SE）的小鼠模型来研究线粒体Rho（MIRO）1在癫痫中的作用。腹腔注射小鼠癫痫患者癫痫发作，在海马中显着降低了Miro 1表达。此外，汲取甘油处理增加了热休克蛋白70（HSP70）和S100钙结合蛋白B（S100B）的血清水平，并导致海马神经元损伤和凋亡。在紫罗兰甘油诱导的SE之后，在海马神经元中激活内在凋亡途径，如裂解的caspase-3和Bcl-2的下调水平增加，以及从线粒体到细胞质的细胞色素C的释放。相比之下，通过腺病毒的侧心室给药的MIRO 1的强迫表达减少了癫痫癫痫发作，降低了HSP70和S100b的升高，并通过抑制了内在的凋亡途径来抑制海马神经元细胞凋亡。总之，我们的数据表明，通过抑制内在的凋亡途径，Miro 1缓解皮脂醛诱导的Se和受保护的海马神经元的异位表达。这些调查结果为癫痫疾病提供了新的见解，并表明Miro 1在治疗癫痫中的潜在神经保护价值。

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