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目的探讨Janus蛋白酪氨酸激酶(JAK)/信号转导和转录激活子1(STAT1)信号转导途径在MRL/lpr狼疮鼠肾脏、肺脏、脑等不同器官中的活化和作用。方法实验组是12周龄以上已经发病的MRL/lpr雌性小鼠．对照组是未发病的同龄MRL/lpr雌性小鼠。采用免疫组织化学方法研究肾脏中磷酸化STAT1的组织分布情况。采用Western blot方法研究STAT1磷酸化蛋白表达,采用SYBR greenⅠre- M-time定量聚合酶链反应(PCR)研究SOCS-1 mRNA的表达；并与肺脏、脑相对比。结果MRL/lpr狼疮鼠STAT1磷酸化蛋白在各器官均明显活化。肾脏和肺脏的STAT1磷酸化蛋白活化较脑组织明显；肾脏、肺脏和脑组织的SOCS-1基因的表达均升高．但肾脏的SOCS-1基因表达升高程度低于肺脏和脑组织。结论JAK/STAT1信号转导途径的异常可能参与和促进了系统性红斑狼疮(SLE)各器官病理损害的发生；狼疮肾炎的病理损害还可能与SOCS-1的负反馈调节作用降低有关。
Objective To investigate the activation and role of Janus protein tyrosine kinase (JAK) / signal transducer and activator of transcription 1 (STAT1) signaling pathways in different organs of kidneys, lungs and brain of MRL / lpr mice. Methods The experimental group was a MRL / lpr female mouse that had developed more than 12 weeks of age. The control group was uninfarmed female mice of the same age MRL / lpr. Immunohistochemistry was used to study the tissue distribution of phosphorylated STAT1 in the kidney. The expression of STAT1 phosphorylation protein was detected by Western blot. The expression of SOCS-1 mRNA was detected by SYBR greenⅠre-M-time quantitative polymerase chain reaction (PCR) and compared with lung and brain. Results MR1 / lpr lupus STAT1 phosphorylation protein in all organs were significantly activated. The activation of STAT1 phosphorylation protein in kidney and lung was more obvious than that in brain tissue. The expressions of SOCS-1 gene in kidney, lung and brain were increased. However, SOCS-1 mRNA expression in the kidneys increased less than in the lungs and brain. Conclusion The abnormal JAK / STAT1 signal transduction pathways may participate in and promote the pathological damage of various organs in systemic lupus erythematosus (SLE). The pathological damage of lupus nephritis may also be related to the decrease of negative feedback regulation of SOCS-1.