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PrP106-126诱导小胶质细胞BV-2抗氧化性能的变化

Altered oxidative stress in BV-2 cells induced by PrP106-126
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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(reactive oxygen species,ROS)进行检测,并通过荧光定量RT-PCR对与ROS相关的酶的mRNA表达进行了测定。结果表明PrP106-126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SOD-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。 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.
出处 《中国兽医学报》 CAS CSCD 北大核心 2013年第12期1802-1807,共6页 Chinese Journal of Veterinary Science
基金 河北省自然科学基金(C2011204059)
关键词 朊病毒 PrP106—126 小胶质细胞BV-2 氧化压力 抗氧化酶 prion PrP106-126 BV-2 microglia ROS antioxidase
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