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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。
Purpose IgA and SC are important components of SIgA. SIgA of intestinal mucosa is an important part of intestinal immune barrier. To understand the pathogenesis of acute liver necrosis, the role of TNF-α in acute liver necrosis and intestinal SIgA changes. Methods Animal model of acute hepatic necrosis was induced by TNF-α / GalN instead of LPS / GaLN. Acute hepatic necrosis induced by LPS / GaLN was blocked by anti-TNF-α and anti-TNF-R1. Immunohistochemistry and Real-time PCR were used to detect the changes of intestinal IgA and SC in the animal model of acute hepatic necrosis. Results TNF-α / GalN induced acute hepatic necrosis. Anti-TNF-α and anti-TNF-R1 blocked acute hepatic necrosis induced by LPS / GaLN. Acute liver necrosis of intestinal tissue IgA, SC was significantly weakened. Conclusion TNF-α plays an important role in the process of acute hepatic necrosis. Acute liver necrosis of intestinal SC, IgA decreased intestinal SIgA decreased intestinal SIgA reduction may be one of the causes of acute hepatic necrosis complicated by spontaneous peritonitis.