Department of Neurology, The Fifth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Department of Neurophysiology, Oilfields General Hospital in Daqing, Daqing, Heilongjiang 163001, P.R. China.
Int J Mol Med. 2018 Sep;42(3):1577-1584. doi: 10.3892/ijmm.2018.3711. Epub 2018 Jun 1.
Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of microRNA-155 in patients with temporal lobe epilepsy. Commercial kit and western blot analysis were used to measure gap-associated protein expression. The aim of the present study was to investigate the effect of microRNA‑155 (miRNA‑155) in the occurrence of epilepsy and the molecular mechanism involved. In patients with temporal lobe epilepsy, miRNA‑155 expression was evidently higher than that in patients of the normal volunteers group. Overexpression of miRNA‑155 resulted in decreased brain‑derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein expression, increased caspase‑3 activity, tumor protein p53 (p53) and apoptosis regulator BAX (Bax) protein expression, and inhibited phosphoinositide 3‑kinase (PI3K), phosphorylated (p‑)protein kinase B (Akt) and p‑mechanistic target of rapamycin (mTOR) protein expression in epilepsy cells. PI3K inhibitor accelerated the effect of miRNA‑155 on the inhibition of BDNF and TrkB protein expression, the promotion of caspase‑3 activity, p53 and Bax protein expression, and the inhibition of PI3K, p‑Akt and p‑mTOR protein expression in epilepsy cells. The present findings indicate that miRNA‑155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway.
逆转录-定量聚合酶链反应（RT-qPCR）用于测量颞叶癫痫患者中 microRNA-155 的表达。商业试剂盒和 Western blot 分析用于测量缝隙连接蛋白的表达。本研究旨在探讨 microRNA-155（miRNA-155）在癫痫发生中的作用及其涉及的分子机制。在颞叶癫痫患者中，miRNA-155 的表达明显高于正常志愿者组。miRNA-155 的过表达导致脑源性神经营养因子（BDNF）和原肌球蛋白受体激酶 B（TrkB）蛋白表达降低，半胱氨酸蛋白酶-3（caspase-3）活性增加，肿瘤蛋白 p53（p53）和凋亡调节因子 BAX（Bax）蛋白表达增加，并且抑制磷酸肌醇 3-激酶（PI3K）、磷酸化蛋白激酶 B（Akt）和机械靶蛋白雷帕霉素（mTOR）蛋白在癫痫细胞中的表达。PI3K 抑制剂加速了 miRNA-155 对 BDNF 和 TrkB 蛋白表达抑制、caspase-3 活性、p53 和 Bax 蛋白表达促进以及 PI3K、p-Akt 和 p-mTOR 蛋白表达抑制的作用在癫痫细胞中。本研究结果表明，miRNA-155 通过 PI3K/Akt/mTOR 信号通路促进癫痫的发生。
