线粒体稳态的维持对保持神经细胞结构和功能的完整性至关重要，进而对改善癫痫患者神经功能及远期预后起着关键作用。沉默microRNA-134被证实对癫痫后神经元损伤具有保护作用，具有广泛的应用前景，但其对癫痫持续状态后海马神经元线粒体稳态的影响及机制尚不清楚。研究发现，抑制线粒体凋亡途径可降低癫痫持续状态导致的海马神经元丢失，并可促进神经细胞线粒体“新生”，而沉默miRNA-134可改善癫痫持续状态后线粒体功能及细胞凋亡。因此，本研究通过建立的大鼠癫痫持续状态损伤模型，在体内研究miRNA-134对神经细胞线粒体稳态（数量、形态、结构），细胞凋亡和神经行为学的影响，并进一步在体外实验阐明沉默miRNA-134是否通过limk /cofilin信号通路调控神经细胞线粒体稳态。深入探讨miRNA-134对癫痫持续状态损伤的作用及关键机制，从而为临床癫痫保护方案的制定提供重要的理论依据。

The maintenance of mitochondrial homeostasis plays a vital role in protecting the structural and functional integrity of the nerve cells.It is of key importance to improve the patients statusepilepticus injury.Silencing miRNA-134 has demonstrated the effective therapy to protect the brain and it has been used in wide range of field.The potential mechanisms of miRNA-134 on mitochondrial homeostasis following statusepilepticus injury are still unclear.Our recent study has shown that Inhibition of the mitochondrial apoptosis pathway can reduce hippocampal neuron loss caused by status epilepticus, and can promote nerve cells mitochondrial "freshman". And silencing miRNA-134 can improve mitochondrial function and cell apoptosis after status epilepticus.Therefore,we investigate the effects of miRNA-134 on neural cells＇mitochondrial homeostasis, outcome of nerve cells and neuroethology using the model of status epilepticus model in rats. Furthemore, we clarify whether silencing miRNA-134 can regulate mitochondrial homeostasis via limk/cofilin signaling pathway.It will provide the important evidence for clinical neuroprotective therapy.