PrP106—126诱导小胶质细胞BV-2抗氧化性能的变化 |
| |
引用本文: | 李玉荣,霍书英,武现军,陈立功,刘静,高玉红.PrP106—126诱导小胶质细胞BV-2抗氧化性能的变化[J].兽医大学学报,2013(12):1802-1807. |
| |
作者姓名: | 李玉荣 霍书英 武现军 陈立功 刘静 高玉红 |
| |
作者单位: | 河北农业大学动物医学院农业部动物疫病病原生物学华北科学观测实验站,河北保定071001 |
| |
基金项目: | 基金项目:河北省自然科学基金(C2011204059) |
| |
摘 要: | 小胶质细胞活化是朊病的病理学特征之一。朊蛋白多肽PrP106—126具神经毒性,是研究异常腕蛋白(PrPSc)的理想工具。为探讨PrP106—126对小胶质细胞氧化压力的影响。本研究以小胶质细胞BV-2为细胞模型,PrP106—126作用48h,应用MTT和流式细胞仪检测细胞的活化情况,应用分子探针技术对细胞的氧化压力(reactiveoxygenspecies,ROs)进行检测,并通过荧光定量RT—PCR对与R0s相关的酶的mRNA表达进行了测定。结果表明PrPl06—126显著促进小胶质细胞BV-2的活化,并提高胞内的ROS水平;定量RT—PCR显示,PrP106—126显著降低细胞S0D-1(P〈0.01)表达水平、提高胞内Cat(P〈0.01)的表达水平;对Grx、Trx-1、和Trx-2mRNA的表达水平有升高的趋势,但未达到显著水平(P〉0.05),对SOd-2、GPx、GR无显著性影响(P〉0.05)。从分子水平初步阐明小胶质细胞ROS升高的机理。
|
关 键 词: | 朊病毒 PrP106—126 小胶质细胞BV-2 氧化压力 抗氧化酶 |
Altered oxidative stress in BV-2 cells induced by PrP106-126 |
| |
Authors: | LI Yu-rong HUO Shu-ying WU Xian-Jun CHEN Li-gong LIU Jing GAO Yu-hong |
| |
Institution: | (College of Veterinary Medicine, Hebei Agricultural University ; North China Research Center of Animal Epi- demic Pathogen Biology ,Ministry of Agricuture of China ,Baoding 071001 ,China) |
| |
Abstract: | Astrogliosis is a hallmark of prion disease, but the metabolic alterations of microglia re- main poorly documented. A synthetic peptide corresponding to amino acid 106-126 of prion protein (PrP) has been shown to be toxic to neurons, and is widely used as a model of PrPso. In this study, the effects of PrP106-126 on BV-2 cell were investigated in vitro. BV-2 microglia added PrP106- 126 significantly increased cell viability and ROS. Further study showed that PrP106-126 treated BV-2 cells had a simultaneous increase in mRNA expression of Cat (P〈0.01),Grx,Trx-1 and Trx-2 mRNA displayed an increasing trend (P〉0.05),but no changes in mRNA expression of SOD-2,GPx and GR were found (P〉0.05) ;the expression of other antioxidant gene SOD-1 was decreased (P〈0.01). This may be partially related to the pathogenesis of prion disease. |
| |
Keywords: | prion PrP106-126 BV-2 microglia ROS antioxidase |
本文献已被 维普 等数据库收录! |