摘要
为观察盲肠结扎穿孔(CLP)所致脓毒症大鼠重要脏器细胞因子信号转导抑制因子 (SOCSs)基因表达的规律及其意义 ,将 5 4只Wistar大鼠随机分为正常对照组 (n =6 )、CLP组 (n=36 )和重组杀菌 /通透性增加蛋白(rBPI2 1)治疗组 (n=12 ) ,检测动物肝、肺、肾组织中SOCS1和SOCS3mRNA的表达 ,同时测定组织中内毒素和TNF α水平。结果显示 ,CLP后肝、肺、肾组织中内毒素和TNF α水平均迅速升高 ,于 2～ 12h达峰值 (P <0 0 5 ) ,其后逐渐降低。脓毒症大鼠肝、肾组织中SOCS1和SOCS3的基因表达均显著升高 ,其中SOCS3基因表达升高迅速且持续时间较长 ,于术后 6h即达到峰值 (P <0 0 5 ) ,72h仍维持于较高水平 ,而肝、肾组织中SOCS1表达呈一过性升高 ,分别于术后 6h和 4 8h显著高于正常对照组 (P <0 0 5 )。rBPI2 1治疗对CLP大鼠肝、肺、肾组织中SOCS1和SOCS3mRNA表达均无显著影响。上述结果提示 ,严重腹腔感染可导致大鼠体内SOCSs表达上调 ,其改变可能与内毒素介导TNF α的刺激作用有关。SOCSs作为内源性细胞内信号转导抑制物在脓毒症的病理生理过程可能发挥了调节作用。
The aim of this study was to observe the changes in tissue suppressors of cytokine signaling (SOCSs) mRNA expression, and to investigate their potential role in the pathogenesis of sepsis induced by cecal ligation and puncture (CLP). Fifty four Wistar rats were randomly divided into three groups: normal control group ( n =6), CLP induced sepsis group ( n =36) and recombinant bactericidal/ permeability increasing protein (rBPI 21 ) treatment group ( n =12). Tissue samples from the liver, lung and kidney were collected to determine SOCS1 and SOCS3 mRNA expressions. Meanwhile, tissue endotoxin and TNF α levels were also determined. The results showed that, after CLP, endotoxin and TNF α levels in the liver, lung and kidney significantly increased, peaking at 2～12h ( P <0 05 or 0 01), then returned to their base lines at 24h. rBPI 21 treatment could effectively reduce endotoxin and TNF α levels in the liver, lung and kidney ( P <0 05 or 0 01). Meanwhile, SOCS1 and SOCS3 mRNA expressions in the liver and kidney were significantly up regulated after CLP. Of them, the changes in SOCS3 mRNA expression were rapid and prolonged, peaking at 6h, and keeping at a high value up to 72h. In contrast, SOCS1 gene expressions in the liver and kidney were transient, peaking at 6h and 48h, respectively. Early treatment with rBPI 21 had no significant effect on the expression of SOCS1 and SOCS3 mRNA in these three organs. These results suggested that severe peritoneal infection could up regulate the gene expressions of SOCSs and SOCSs in vital tissues, which acting as negative regulators of cytokine signaling might play a role in regulating the balance of inflammatory response in abdominal sepsis.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2002年第9期767-769,共3页
Medical Journal of Chinese People's Liberation Army
基金
国家重点基础研究发展规划项目 (编号G1 9990 542 0 3)
国家杰出青年科学基金 (编号 30 1 2 50 2 0 )
军队杰出中青年人才专项基金 (编号 98J0 1 3)资助课题
