PrP106—126诱导小胶质细胞BV-2抗氧化性能的变化

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。

Altered oxidative stress in BV-2 cells induced by PrP106-126

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.