细胞因子信号抑制因子3在小鼠肾炎进程中的表达

Expression of suppressor of cytokine signaling 3 during the course of mouse nephritis

目的:探索细胞因子信号抑制因子3(SOCS3)在小鼠肾炎进程中的表达变化规律和意义。方法:采用含兔抗小鼠肾小球基底膜抗体的肾毒素血清(NTS)制备小鼠肾炎模型。在第10、15、20和25 d分别收集小鼠尿液并摘取肾脏。以蛋白尿水平、肾脏组织HE和Masson染色评价肾炎进程;采用免疫组化和Western blotting法检测SOCS3蛋白表达变化,以及Janus激酶2(JAK2)和信号转导及转录激活因子3(STAT3)在小鼠肾炎进程中磷酸化情况。结果:小鼠肾炎模型表现出典型的发病、进展与转归;SOCS3在肾炎进程中未出现立即随JAK2和STAT3磷酸化增多而表达增加的现象,仅在肾炎严重期(第20 d)表达增加(P<0.05),在恢复期(第25 d)表达明显增加(P<0.01)。恢复期SOCS3表达显著增加,表现出抑制JAK2和STAT3磷酸化的作用。结论:机体自身条件下,SOCS3的表达未立即随JAK2/STAT3磷酸化增多而增加,SOCS3对免疫性肾炎的保护作用可能主要在肾炎恢复期。

AIM： To explore the expression and role of suppressor of eytokine signaling 3 （SOCS3） in mouse nephritis. METHODS： C57BL/6 mice were challenged with rabbit anti -mouse glomerular basement membrane nephro- toxic sera （NTS） to induce immune nephritis. On days 10, 15, 20 and 25, the urine samples from the mice were collect- ed, and the kidneys were also harvested. The degree of proteinuria and the changes of renal pathology were detected to as- sess the course of nephritis. The expression of SOCS3 and the phosphorylation of Janus kinase 2 （JAK2） and signal trans- ducer and activator of transcription 3 （STAT3） in the kidney were determined by Western blotting and immunohistochemi- cal method. RESULTS： In model group, the severity of pathological changes increased over time by determining the pro- teinurla levels and observing the kidney pathological sections. However, the nephritis was improved on day 2.5. The expres- sion level of SOCS3 did not change with the phosphorylation of JAK2/STAT3 immediately, but became increased when the disease was severer and got to a significantly higher level in convalescence. CONCLUSION： The expression level of SOCS3 does not increase immediately after the remarkable phosphorylation of JAK2/STAT3, and the protective effect of SOCS3 in nephritis might occur in convalescence.