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目的探讨氯化锂预处理对脂多糖诱导的BV-2小胶质细胞炎症反应的影响及其作用机制。方法体外培养小鼠BV-2小胶质细胞株,用脂多糖1.0 g/ml(A组)、氯化锂10mmol/L(B组)或两药联用(C组)刺激BV-2细胞12h,以不加药物作对照(D组)。采用实时FQ-PCR法检测各组细胞中炎症因子IL-1β和TNF-αmRNA表达量,Western blot法检测磷酸化糖原合成酶激酶3β(pGSK-3β)表达量。结果与D组比较,A组和C组BV-2细胞IL-1β和TNF-αmRNA表达量及pGSK-3β表达量均增加(P<0.05)。与A组比较,C组IL-1β和TNF-αmRNA表达量减少(P<0.05),pGSK-3β表达量增加(P<0.05)。结论氯化锂可以减轻脂多糖诱导的小胶质细胞炎症反应,其机制可能与GSK-3β通路有关。
Objective To investigate the effect of lithium chloride pretreatment on lipopolysaccharide-induced BV-2 microglial inflammatory reaction and its mechanism. Methods BV-2 microglia cell lines were cultured in vitro. BV-2 cells were stimulated with lipopolysaccharide 1.0 g / ml (group A), lithium chloride 10 mmol / L (group B) 12h, with no drug as a control (D group). The expression of IL-1β and TNF-α mRNA in each group were detected by real-time FQ-PCR. The expression of phosphorylated glycogen synthase kinase 3β (pGSK-3β) was detected by Western blot. Results Compared with group D, the expression of IL-1β and TNF-α mRNA and the expression of pGSK-3β in BV-2 cells of group A and group C were increased (P <0.05). Compared with group A, the expression of IL-1β and TNF-α mRNA in group C decreased (P <0.05) and the expression of pGSK-3β increased (P <0.05). Conclusion Lithium chloride can reduce lipopolysaccharide-induced microglial inflammatory response, the mechanism may be related to GSK-3β pathway.