中文摘要：

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。

英文摘要：

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.