作者: Teng Ma , Xiyan Wu , Qiyan Cai , Yun Wang , Lan Xiao
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摘要: Lead (Pb) poisoning has always been a serious health concern, as it permanently damages the central nervous system. Chronic Pb accumulation in human body disturbs oligodendrocytes (OLs) differentiation, resulting dysmyelination, but molecular mechanism remains unknown. In this study, at 1 μM inhibits OLs precursor cells (OPCs) differentiation via decreasing expression of Olig 2, CNPase proteins vitro. Moreover, treatment sodium/calcium exchanger 3 (NCX3) mRNA expression, one major means calcium (Ca2+) extrusion plasma membrane during OPCs differentiation. Also addition KB-R7943, NCX3 inhibitor, to simulate toxicity, resulted decreased myelin basic protein (MBP) and cell branching. Ca2+ response trace with KB-R7943 did not drop down same recovery time control, which elevated intracellular concentration reducing MBP expression. contrast, over-expression exposed displayed significant increase fluorescence signal positive regions recovered counterbalance toxicity. conclusion, exposure affecting function by inducing overload.