MiR-134在MA诱导神经元损伤中的表达及其对神经诱发动作电位的影响

发布时间：2018-04-06 23:14

本文选题：miR-　切入点：甲基苯丙胺　出处：《中山大学学报(医学科学版)》2017年01期

【摘要】：【目的】探讨微小非编码RNA分子miR-134在甲基苯丙胺(MA)诱导PC12神经细胞损伤中的表达变化及其对神经兴奋性的影响,为理解MA导致神经损伤的机制提供实验基础。【方法】将处于对数生长期的PC12细胞分为对照组和MA组。MA组应用800μmol/L MA处理,建立体外神经元损伤模型,观察培养神经细胞损伤及细胞凋亡情况;采用实时荧光定量PCR技术测定miR-134的表达水平变化;并构建miR-134干扰载体,抑制miR-134后分析神经诱发动作电位的变化。【结果】MA可明显诱导PC12细胞损伤,神经突起变短,细胞凋亡数目增多;荧光定量PCR结果显示miR-134表达升高;电生理学检测结果显示,干扰miR-134后诱发动作电位增多。【结论】高浓度MA诱导神经细胞损伤、诱发神经元凋亡并升高miR-134表达,沉默miR-134表达,可增加神经兴奋性。本实验为阐明MA的神经损伤机制,以及miR-134在神经元毒性损伤及神经兴奋性中的可能作用提供了实验依据。
[Abstract]:[objective] to investigate the changes of miR-134 expression in PC12 neurons induced by methamphetamine (MA) and its effect on neuronal excitability.[methods] PC12 cells in logarithmic growth phase were divided into control group and MA group treated with 800 渭 mol/L MA to establish neuronal injury model in vitro.The damage and apoptosis of cultured neurons were observed, the expression of miR-134 was measured by real-time fluorescence quantitative PCR, and the interference vector of miR-134 was constructed.After inhibition of miR-134, the changes of nerve evoked action potential were analyzed. [results] MA could obviously induce PC12 cell injury, the neurite became shorter and the number of apoptosis increased; fluorescence quantitative PCR showed that the expression of miR-134 was increased; electrophysiological test showed that,[conclusion] High concentration of MA can induce neuronal injury, induce neuronal apoptosis and increase the expression of miR-134, and silence the expression of miR-134, which can increase the neuronal excitability.This study provides experimental basis for elucidating the mechanism of MA nerve injury and the possible role of miR-134 in neuronal toxicity and neuronal excitability.
【作者单位】：济南市第四人民医院神经外科;山东大学医学部解剖与组胚研究所;
【基金】：山东省医药卫生科技发展项目(2013WS008) 山东省重点研发计划(2016GSF201054)
【分类号】：R741

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