溃疡性结肠炎组织中SOCS2、SOCS3表达量与炎症反应、免疫应答的相关性

Expression of SOCS2 and SOCS3 in ulcerative colitis and its correlation with inflammatory response and immune response

目的:研究溃疡性结肠炎组织中SOCS2、SOCS3表达量与炎症反应、免疫应答的相关性。方法:选择2014年5月~2016年7月期间在淄矿集团中心医院结肠镜活检的溃疡性结肠炎病灶组织和正常肠黏膜组织,分别作为UC组和对照组。抽提RNA并测定SOCS2、SOCS3以及炎症反应JAKs/STATs通路分子的mRNA表达量,抽提蛋白并测定免疫应答细胞因子的含量。结果:UC组肠黏膜组织中SOCS2的mRNA表达量与对照组比较差异无统计学意义(P>0.05),SOCS3的mRNA表达量显著低于对照组;UC组肠黏膜组织中JAK1、JAK2、JAK3、STAT1、STAT3、STAT5的mRNA表达量以及γ干扰素(IFN-γ)、白介素(IL)-17的蛋白含量显著高于对照组,IL-4、IL-10的蛋白含量显著低于对照组;UC组中SOCS3低表达肠黏膜组织中JAK1、JAK2、JAK3、STAT1、STAT3、STAT5的mRNA表达量以及IFN-γ、IL-17的蛋白含量显著高于SOCS3高表达肠黏膜组织,IL-4、IL-10的蛋白含量显著低于SOCS3高表达肠黏膜组织。结论:溃疡性结肠炎组织中低表达的SOCS3能够加重炎症反应、造成Th1/Th2以及Th17/Treg免疫应答失衡。

Objective： To study the correlation between the expression of SOCS2 and SOCS3 in ulcerative colitis with inflammatory response and immune response.Methods： ulcerative colitis lesions and normal mucosa from colonoscopic biopsy in Central Hospital of Zibo mining Refco Group Ltd during May 2014-July 2016, respectively as UC group and control group.RNA was extracted and mRNA expression of SOCS2, SOCS3 and inflammatory response JAKs/STATs pathway were determined;protein was extracted and the content of immune response cytokines was determined.Results： mRNA expression of SOCS2 in intestinal mucosa of UC group had no difference with control group, SOCS3 mRNA expression was significantly lower than the control group;mRNA expression of JAK1, JAK2, JAK3, STAT1, STAT3, STAT5 and protein contents of IFN-γ, IL-17 in intestinal mucosa of UC group were significantly higher than control group, protein contents of IL-4, IL-10 were significantly lower than control group;mRNA expression of JAK1, JAK2, JAK3, STAT1, STAT3, STAT5 in SOCS3 low expression intestinal mucosa of UC group were significantly higher than SOCS3high expression intestinal mucosa, protein content of IL-4 and IL-10 were significantly lower than t SOCS3 high expression intestinal mucosa.Conclusions： low expression of SOCS3 in ulcerative colitis can aggravate the inflammatory reaction;cause the imbalance of Th1/Th2 and Th17/Treg immune response.