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目的探讨细胞因子信号转导抑制因子-1和3(SOCS1和SOCS3)的含量在脓毒症小鼠脾脏中的变化情况以及可能的作用机制。方法采用盲肠结扎并穿刺术(CLP)制作脓毒症模型,提取脾脏组织的RNA及蛋白质,采用RT-PCR测定组织中SOCS1和SOCS3 mRNA的相对含量,用免疫印迹方法测定组织中SOCS1和SOCS3相对蛋白含量,用SPSS统计软件测定上述指标之间的变化关系。结果脓毒症手术后SOCS1在脾脏中仅检测到基因表达,随时间逐渐上升,并一直保持高位;SOCS3在脾脏内的基因表达和蛋白表达在术后2h迅速升高,至12h达峰值(P<0.05);统计分析发现SOCS1和SOCS3的基因表达呈明显正相关性(P<0.05)。结论 CLP导致的脓毒症可以诱导SOCS1和SOCS3在脾脏中表达增多,提示SOCS1和SOCS3在脓毒症出现后的免疫变化中有重要作用,可能可利用它们对脓毒症进行干预,以改善脓毒症的预后。
Objective To investigate the changes of cytokine signaling inhibitors 1 and 3 (SOCS1 and SOCS3) in the spleen of septic mice and the possible mechanism. Methods Sepsis model was made by cecal ligation and puncture (CLP). RNA and protein of spleen tissues were extracted. The relative contents of SOCS1 and SOCS3 mRNA in tissues were determined by RT-PCR. The relative expression of SOCS1 and SOCS3 in tissues was determined by Western blotting Protein content, using SPSS statistical software to determine the relationship between the above changes. Results Only the expression of SOCS1 was detected in the spleen after sepsis surgery, and the expression of SOCS1 in the spleen increased rapidly with the rise of time. The expression of SOCS3 in the spleen increased rapidly at 2 hours and reached the peak at 12 hours (P <0.05). Statistical analysis showed that the gene expressions of SOCS1 and SOCS3 were positively correlated (P <0.05). Conclusions CLP-induced sepsis can induce an increase in the expression of SOCS1 and SOCS3 in the spleen, suggesting that SOCS1 and SOCS3 play an important role in the immune changes following sepsis and may be used to intervene in sepsis to improve pus The prognosis of the disease.