PI3K/Akt通路调节LPS诱导的小胶质细胞内HSPA12B表达

摘要

Objective:To explore the effect of PI3K/Akt on the expression of Heat shock protein A 12B(HSPA12B) synthase protein in rat microglias induced by lipopolysaccharide(LPS).Methods:Microglias were divided into three groups:control group,0.1 μg/ml LPS stimulation group,pretreatment PI3K/Akt inhibitor before LPS stimulation group.Western blot measurement was used to observe the expressions of HSPA12B protein and phosphorylated Akt.Intracellular location of HSPA12B was detected under fluorescence microscope.Results:HSPA12B protein and phosphorylated Akt increased after 2 h exposure to LPS.The LPS-induced HS-PA12B protein expression was strongly decreased when the cells were pretreated with PI3K/Akt inhibitor LY294002.Immunocytochemical staining indicated that the expression of HSPA12B was located in the nuclear following LPS chal-lenge.LY294002 resulted in the weakened intensity of fluorescence in the cells.Conclusion:PI3K/Akt signaling pathway was involved in LPS-induced the expression of HSPA12B protein in rat microglias.%目的:探讨PI3K/Akt通路对内毒素脂多糖(Lipopolysaccharide,LPS)诱导的小胶质细胞内热休克蛋白A12B (Heat shock proteins A 12B,HSPA12B)表达的影响.方法:体外培养小胶质细胞,并分三组处理:对照组、0.1 μg/ml LPS刺激组、PI3K/Akt通路抑制LPS刺激组.Western blot法检测小胶质细胞内HSPA12B和Akt磷酸化的蛋白水平表达,间接免疫荧光标记法检测HSPA12B在小胶质细胞中的细胞表达定位.结果:LPS刺激2 h后,小胶质细胞内HSPA12B和Akt磷酸化的表达增加;应用LY294002预处理后,LPS诱导HSPA12B蛋白水平表达显著抑制.免疫细胞荧光染色证明小胶质细胞LPS组HSPA12B核周荧光强度明显增强,LY294002预处理组HSPA12B荧光强度明显减弱.结论:PI3K/Akt途径参与调控LPS诱导小胶质细胞HSPA12B表达.