PI3K/AKT信号通路在SjCystatin诱导M2巨噬细胞分化过程中的影响  

Effects of PI3K/AKT signaling pathway on polarization of M2 macrophages induced by SjCystatin

作　　者：刘炬[1] 杨潇[1] 岳媛[1] 王乐旬[1] 吴钟凯[1] 

机构地区：[1]中山大学附属第一医院心外二科,广东广州510080

出　　处：《中国病理生理杂志》2016年第6期971-977,共7页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81570039);广东省自然科学基金资助项目(No.S2013040012612)

摘　　要：目的:进一步确定日本血吸虫半胱氨酸蛋白酶抑制剂(Sj Cystatin)诱导M2巨噬细胞分化的亚型及相关机制。方法:用ELISA、RT-q PCR或Western blot法测定IL-10、IL-12、巨噬细胞亚型表面标志物LIGHT(M2b)及Arg-1(M2a+M2c)的表达;用Western blot法测定AKT的磷酸化水平。结果:Sj Cystatin处理组在6 h、12 h和24h时IL-10表达量持续增加;处理12 h,LIGHT的mRNA和蛋白表达量增加但Arg-1的mRNA和蛋白表达量降低;AKT磷酸化水平增加。PI3K/AKT抑制剂处理组IL-10的释放量在12 h和24 h持续降低;24 h,LIGHT的mRNA和蛋白表达量降低但Arg-1的mRNA和蛋白表达量增加;AKT的磷酸化水平减少。结论:Sj Cystatin促进了活化的M2巨噬细胞分化为M2b亚型巨噬细胞,并且PI3K/AKT信号通路参与了这一过程。AIM： To investigate the subtype of M2 macrophages induced by Schistosoma japonicum cystatin（ Sj Cystatin） and to determine the mechanism underlying these effects. METHODS： The releases of IL-10 and IL-12,and the expression of macrophage subtype markers LIGHT（ M2b） and Arg-1（ M2 a ＋ M2c） were assessed by ELISA,RTq PCR and Western blot. The phosphorylation level of AKT was assessed by Western blot. RESULTS： Sj Cystatin promoted the continuous increase in IL-10 level at 6 h,12 h and 24 h,and increased the amount of mRNA and protein expression of LIGHT,but down-regulated the amount of mRNA and protein expression of AKT. The addition of PI3 K / AKT inhibitor reduced the release of IL-10 at 12 h and 24 h,reduced the mRNA and protein expression of LIGHT at 24 h,up-regulated the mRNA and protein expression of Arg-1 at 24 h,and decreased the phosphorylation level of AKT. CONCLUSION： Sj Cystatin promotes the differentiation of M2 macrophage to M2 b macrophage subtype,and the PI3 K / AKT signaling pathway is involved in this process.

关 键 词：半胱氨酸蛋白酶抑制剂 M2b巨噬细胞 M2巨噬细胞 PI3K/AKT信号通路 

分 类 号：R392.21[医药卫生—免疫学] R363[医药卫生—基础医学]