在急性肝坏死中TNF-α的作用和肠道IgA、SC的变化(英文)  

The role of TNF-α and the change of intestinal IgA, SC in acute liver necrosis

作　　者：刘冬妍[1] 曹旭[1] 周潇男[2] 刘沛[3] 

机构地区：[1]中国医科大学附属盛京医院实验研究中心卫生部小儿先天畸形重点实验室,辽宁沈阳110004 [2]中国医科大学,临床医学94期辽宁沈阳110001 [3]中国医科大学附属第一医院感染科,辽宁沈阳110001

出　　处：《中国现代医学杂志》2012年第30期1-8,共8页China Journal of Modern Medicine

基　　金：国家自然基金资助项目(No:30871158;81170604);盛京自由研究者基金

摘　　要：目的 IgA和SC是SIgA的重要组成,肠黏膜的SIgA是肠免疫屏障重要组成部分。为了解急性肝坏死的发病原因,研究TNF-α在急性肝坏死中的作用和肠道SIgA变化。方法用TNF-α/GalN代替LPS/GaLN诱导急性肝坏死动物模型,用Anti-TNF-α和anti-TNF-R1封闭由LPS/GaLN诱导的急性肝坏死。采用免疫组化方法和Real-time PCR方法检测急性肝坏死动物模型肠道IgA、SC的变化。结果TNF-α/GalN诱导了急性肝坏死,Anti-TNF-α和anti-TNF-R1封闭了由LPS/GaLN诱导急性肝坏死。急性肝坏死肠组织IgA、SC明显减弱。结论 TNF-α在急性肝坏死过程中发挥重要作用。急性肝坏死肠道SC、IgA减少导致肠道SIgA的减少,肠道SIgA的减少可能是急性肝坏死并发自发性腹膜炎的原由之一。[ Objective ] gA and secretory component （SC） are key components of Secretory IgA （SIgA）. SIgA of intestinal mucosa is an important factor of intestinal immunology barrier. To know the cause of acute liver necrosis, the change of intestinal SIgA and the role of TNF-ct in the acute liver necrosis were studied. [Methods] LPS/D- GaIN was replaced by TNF-α/D-GalN to induce acute liver necrosis. Anti-TNF-ct and anti-TNF-Rl were used to block the acute liver necrosis induced by LPS/D-GalN. Immunohistochemistry, Quantitative real-time PCR were used to detect intestinal tissue IgA, SC. [Results] The acute liver necrosis could be induced by TNF-cdl）-GalN. The acute liver necrosis induced by LPS/D-GalN may be block by anti-TNF-ct and anti-TNF-R1. Intestinal IgA and SC in acute liver necrosis were remarkably decreased. [Conclusion] TNF-α played an crux role in acute liver necrosis. The lower intestinal IgA and SC （SIgA） in acute liver necrosis induced intestinal SIgA decrease. The lower intestinal SIgA levels would be an important factor tO lead to SBP in acute liver necrosis.

关 键 词：肿瘤坏死因子 免疫球蛋白A 分泌片 肠道 急性肝坏死 

分 类 号：R285.5[医药卫生—中药学]