Gong Lina, Yang Pu, Hu Ling, Zhang Chen
Department of Neurology, The Third Xiangya Hospital of Central South University Changsha 410013, Hunan, China.
Am J Transl Res. 2020 Jun 15;12(6):2769-2780. eCollection 2020.
Epilepsy (EP) is a very dangerous neurological disease. MiR-181b was reported to play a regulatory role during the progression of EP. However, the mechanism by which miR-181b regulates the process of EP remains unclear.
Hippocampal neurons were extracted from rats, which were treated with magnesium-free to mimic EP . CCK-8 assay was performed to test the cell viability. Gene and protein expressions in hippocampal neurons were detected by qRT-PCR, immunofluorescence and western blot, respectively. In addition, TUNEL staining was performed to test the cell apoptosis. Finally, dual luciferase report assay was used to verify the relation between miR-181b, ZNF883 and RASSF1A.
Magnesium-free significantly inhibited the proliferation of hippocampal neurons, which was reversed by miR-181b mimics. In consistent, magnesium-free induced apoptosis of cells was notably inhibited by miR-181b mimics. In addition, miR-181b suppressed the progression of EP via directly targeting RASSF1A and activating PI3K/Akt signaling. Finally, upregulation of miR-181b notably suppressed the progression of EP via regulation of ZNF883.
MiR-181b suppressed the progression of epilepsy via regulation of RASSF1A and lncRNA ZNF883. Thus, miR-181b might serve as a new target for treatment of EP.
癫痫（EP）是一种非常危险的神经系统疾病。据报道，miR-181b在EP进展过程中发挥调节作用。然而，miR-181b调节EP进程的机制仍不清楚。
从大鼠中提取海马神经元，用无镁培养基处理以模拟癫痫。进行CCK-8检测以测试细胞活力。分别通过qRT-PCR、免疫荧光和蛋白质印迹检测海马神经元中的基因和蛋白质表达。此外，进行TUNEL染色以检测细胞凋亡。最后，使用双荧光素酶报告基因检测来验证miR-181b、ZNF883和RASSF1A之间的关系。
无镁培养基显著抑制海马神经元的增殖，miR-181b模拟物可逆转这种抑制作用。同样，miR-181b模拟物可显著抑制无镁培养基诱导的细胞凋亡。此外，miR-181b通过直接靶向RASSF1A并激活PI3K/Akt信号通路来抑制EP的进展。最后，miR-181b的上调通过调节ZNF883显著抑制EP的进展。
miR-181b通过调节RASSF1A和长链非编码RNA ZNF883来抑制癫痫的进展。因此，miR-181b可能成为治疗EP的新靶点。
