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目的观察肝脏X受体非选择性激动剂TO901317对酒精致新生小鼠大脑白质内炎症反应的调节作用。方法分别采用少突胶质前体细胞标记物血小板源性生长因子受体α(PDGFR-α),星形胶质细胞标记酸性纤维胶原蛋白(glial fibrillary acidprotein,GFAP),小胶质细胞标记物(tomato-lectin),运用免疫组织化学方法检测LXR激动剂TO901317对出生后第6天(P6)酒精致小鼠大脑胼胝体处白质炎症反应的作用及少突胶质前体细胞的调节作用。结果新生小鼠(P5)酒精暴露使脑白质处PDGFR-标记的少突胶质前体细胞数量显著减少(P<0.01),而GFAP标记的星形胶质细胞数量和tomato-lectin标记的小胶质细胞数量显著增加(P<0.01),TO901317预处理导致酒精暴露新生小鼠大脑白质PDGFR-α阳性细胞数量明显高于单纯酒精注射组(P<0.01),而GFAP,tomato-lectin阳性细胞数量明显低于单纯酒精注射组(P<0.01)。结论 LXR受体激活能有效抑制大脑白质神经炎症反应,并促进少突胶质前体细胞存活。
Objective To observe the regulatory effect of hepatic X receptor non-selective agonist TO901317 on inflammatory reaction in the white matter induced by alcohol in neonatal mice. Methods The expression of PDGFR-α, glial fibrillary acid protein (GFAP), microglial marker To detect the effect of LXR agonist TO901317 on the white matter inflammatory response induced by alcohol and the regulation of oligodendrocyte precursors on the 6th day after birth in mice by immunohistochemistry. Results Alcohol exposure of neonatal mice (P5) significantly reduced the number of PDGFR-labeled oligodendrocyte precursors (P <0.01), while the number of GFAP-labeled astrocytes and the number of tomato-lectin-labeled small The number of glial cells significantly increased (P <0.01). The number of PDGFR-α positive cells in white matter of neonatal mice exposed to TO901317 pretreatment was significantly higher than that of the ethanol injection group (P <0.01), while GFAP, tomato-lectin positive cells The number was significantly lower than the simple alcohol injection group (P <0.01). Conclusion LXR receptor activation can effectively inhibit white matter neuroinflammation and promote oligodendrocyte precursor cell survival.