17β-雌二醇抑制高氧所致少突前体细胞凋亡

17β-estradiol suppresses hyperoxia-induced apoptosis of oligodendrocyte precursor cells through paired-immunoglobulin-like receptor B

摘要:

目的 探讨高氧及配对免疫球蛋白样受体B （PirB）对大鼠体外少突前体细胞 （OPCs）的影响，以及17β雌二醇 （E2）的保护作用。方法 用逆转录定量酶联反应 （RT-qPCR）检测OPCs的PirB mRNA和蛋白表达，用siRNA沉默OPCs的PirB，高氧刺激后再用E2处理，通过3- （4,5-二甲基噻唑-2）-2,5-二苯基四氮唑溴盐 （MTT）比色法和流式细胞术测定OPCs细胞存活率和凋亡率。结果 高氧导致OPCs凋亡增加和活性降低，E2能够明显下调PirB的表达，E2处理或沉默PirB能够明显减少高氧所致的OPCs凋亡、增加细胞存活率。结论 高氧导致OPCs的凋亡，而E2能够保护高氧所致的OPCs凋亡。

Abstract:

Objective To study the effect of hyperoxia and paired immunoglobin-like receptor B (PirB) on rat oligodendrocyte precursor cells (OPCs) in vivo and the neuroprotective effects of 17β-estradiol (E2) on these cells. Methods Rat OPCs were treated with different concentrations of E2 and the cells were harvested for RT-qPCR analysis at different time points. PriB was silenced with small interfering siRNA. The effects of E2 treatment and silencing of PriB on OPCs viability and apoptosis under hyperoxic stimulation were detected using 3-(4,5-dimethylthi-azol-2-yl)-2 ,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis. Results Hyperoxia induced apoptosis in OPCs and decreased their viability. E2 treatment markedly down-regulated the expression of PirB. E2 treatment or PirB silencing markedly decreased hyperoxia-induced apoptosis and increased cell viability in OPCs. Conclusions E2 can protect OPCs from hyperoxia-induced apoptosis.