期刊文献+

细胞因子信号转导抑制因子-1在脓毒症小鼠肝脏和脾脏中表达的研究 被引量:3

Study on the expression of supressors of cytokine signaling - 1 in liver and spleen of septic mice
暂未订购
导出
摘要 目的观察细胞因子信号转导抑制因子-1(SOCS1)在脓毒症小鼠肝脏和脾脏中的变化情况,探讨SOCS在体内的可能作用机制。方法采用盲肠结扎穿孔术(CLP)制备脓毒症小鼠模型。提取肝脏和脾脏组织的总RNA及蛋白,采用逆转录-聚合酶链反应(RT—PCR)技术测定组织中SOCS1 mRNA的相对含量;用免疫印迹法测定组织中SOCS1相对蛋白含量;用SPSS统计软件分析上述指标之间的变化关系。结果脓毒症小鼠术后6h肝组织SOCS1的基因和蛋白表达均迅速升高,基因表达至24h达到高峰(P〈0.05),蛋白表达一直保持高位;在脾脏中仅检测到SOCS1基因表达,随时间延长逐渐上升,并一直保持高位;肝脏中SOCS1的基因和蛋白表达量间呈明显正相关(y=0.110±5.765×10&-3x,r=0.837,F=93.309,P〈0.01)。结论CLP导致的脓毒症可诱导SOCS1在肝脏和脾脏中进一步表达,提示SOCS1在脓毒症出现后的免疫变化中有重要作用,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 change in supressors of cytokine signaling - 1 (SOCS1) gene in the liver and the spleen of septic mouse, and to find out its probable mechanisms of action in sepsis. Methods Cecal ligation and puncture (CLP) was adopted to reproduce sepsis model. The liver and the spleen tissues were harvested and RNA and protein were respectively extracted. The contents of the regulatory genes SOCS1 mRNA were determined by reverse transcription -polymerase chain reaction (RT - PCR) and regulatory content of protein was detected by Western blotting. The SPSS statistics software was adopted to calculate the correlation. Results The expressions of SOCS1 on gene and protein in the liver were markedly upregulated at 6 th hour. The gene expression peaked at the 24 th hour (P〈0.05). The expression of protein was persistently high. However, the expression of SOCS1 was only detected in the spleen, and it obviously rose in strength with the passage of time, and it remained in a high level. By statistical analysis, positive correlations were found between the gene and protein expressions of SOCS1 (y=0. 110±5. 765× 10^-3x, r=0. 837, F= 93. 309, P〈0.01). Conclusion CLP induced sepsis can induce the up - regulation of the expressions of SOCS1, indicating that SOCS1 play important role in the change in immune system in sepsis. They may be used to intervene sepsis so as to improve the outcome of sepsis.
出处 《中国危重病急救医学》 CAS CSCD 北大核心 2007年第10期606-609,共4页 Chinese Critical Care Medicine
基金 广东省广州市科委重点攻关课题(2001-Z-130-02) 广东省医学科研基金资助项目(A2003176)
关键词 脓毒症 细胞因子信号转导抑制因子 肝脏 脾脏 sepsis supressors of cytokine signaling - 1 liver spleen
  • 相关文献

参考文献14

  • 1马中富,乐胜,梁艳冰,詹红,唐皓,荆小莉.p38丝裂原活化蛋白激酶抑制剂对脓毒症大鼠多器官损伤的保护作用研究[J].中国危重病急救医学,2005,17(4):211-213. 被引量:18
  • 2Ebong S, Call D, Nemzek J,et al. Immunopathologic alterations in murine models of sepsis of increasing severity [J]. Infect Immun, 1999,67(12) : 6603 - 6610.
  • 3Ayala A,Chaudry I H. Immune dysfunction in murine polymicrobial sepsis:mediators macrophages lymphocytes and apoptosis [J]. Shock,1996,6(Suppl 1):S27 - 38.
  • 4Berlato C, Cassatella M A, Kinjyo I, et al. Involvement of suppressor of cytokine signaling - 3 as a mediator of the inhibitory effects of IL - 10 on lipopolysaccharide - induced macrophage activation [J]. J Immunol, 2002, 168 (12): 6404 - 6411.
  • 5Nakagawa R,Naka T,Tsutsui H,et al. SOCS- 1 participates in negative regulation of LPS responses [J]. Immunity, 2002, 17 (5):677 -687.
  • 6Kinjyo I, Hanada T,Inagaki-Ohara K,et al. SOCS1/JAB is a negative regulator of LPS- induced macrophage activation [J]. Immunity,2002,17(5) :583 - 591.
  • 7Egwuagu C E,Yu C R,Zhang M,et al. Suppressors of cytokine signaling proteins are differentially expressed in Thl and Th2 cells., implications for Th cell lineage commitment and maintenance[J]. J Immunol,2002,168(7) :3181 - 3187.
  • 8Ketteler R, Moghraby C S, Hsiao J G, et al. The cytokine - inducible Scr homology domain -containing protein negatively regulates signaling by promoting apoptosis in erythroid progenitor cells[J]. J Biol Chem,2003,278(4) :2654 - 2660.
  • 9Hotchkiss R S,Tinsley K W,Swanson P E,et al. Sepsis - induced apoptosis causes progressive profound depletion of B and CD4^+ T lymphocytes in humans [J]. J Immunol, 2001,166 (11) : 6952 - 6963.
  • 10Saito H,Morita Y,Fujimoto M,et al. IFN regulatory factor - 1 mediated transcriptional activation of mouse STAT induced STAT inhibitor- 1 gene promoter by IFN - gamma [J]. J Immunol,2000,164(11) :5833 - 5843.

二级参考文献12

  • 1Hale K K,Trollinger D,Rihanek M,et al.Differential expression and activation of p38 mitogen-activated protein kinase alpha,beta,gamma,and beta in inflammatory cell lineages[J].J Immunol 1999,162:4246-4252.
  • 2Symons J A,Young P R,Duff G W.Soluble typeⅡ interleukin-1(IL1) receptor binds and blocks processing of IL-1 beta precursor and loses affinity for IL-1 receptor antagonist[J].Proc Natl Acad Sci USA,1995,92:1714-1718.
  • 3Reinhart K,Wiegand Lohnert C,Grimminger F,et al.Assessment of the safety and efficacy of the monoclonal anti tumor necrosis factor antibody fragment,MAK195F,in patients with sepsis and septic shock:a multicenter,randomized,placebo controlled,dose ranging study[J].Crit Care Med,1996,24:742-773.
  • 4Lee J C,Kassis S,Kumar S,et al.p38 mitogen activated protein kinase inhibitor-mechanisms and therapeutic potentials[J].Pharmacol Ther,1999,82:389-397.
  • 5Obata T,Brown G E,Yaffe M B.MAP kinase pathways activation bu stress:the p38 MAPK pathway[J].Crit Care Med,2000,28:N67-N77.
  • 6Branger J,van den Blink B,Weijer S,et al.Anti-inflammatory effects of a p38 mitogen-activated protein kinase inhibitor during human endotoxemia[J].J Immunol,2002,168:4070-4077.
  • 7Nick J A,Avdi N J,Young S K,et al.An intracellular signaling pathway linhing lipopolysaccaride stimulation to cellular responses of the human neitrophil:thr p38 MAP kinase cascade and its functional significance[J].Chest,1999,116(1Suppl):54S-55S.
  • 8Ono K,Han J.The p38 signal transduction pathway:activation and function[J].Cell Signal,2000,12:1.
  • 9姚咏明,盛志勇.MODS抗炎治疗研究的反思[J].中国危重病急救医学,1999,11(8):456-458. 被引量:74
  • 10梁华平,王正国,朱佩芳.针对SIRS的新型抗炎靶点及抗炎策略研究进展——从炎症介质到核因子-κB[J].中国危重病急救医学,2001,13(11):649-652. 被引量:34

共引文献17

同被引文献19

引证文献3

二级引证文献21

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部