免疫复合物型肾小球肾炎发病机制动物实验研究

Animal Experimental Study of Pathogenesis of ICGN

本文按Ｄｉｘｏｎ方法制造血清病型肾小球肾炎动物模型，进而研究发病机制。模型ＡＥＳＳＲ血清ＣＩＣ水平明显高于正常值（Ｐ＜０．０１）；ＣＭＳＣ水平明显低于正常值（Ｐ＜０．０１）．ｓＩＬ－２Ｒ、ＩＬ－８、ＩＦＮ、ＴＮＦ和ＩＬ－２水平均明显高于正常值（Ｐ＜０．０１）。ＣＩＣ与ＣＭＳＣ呈高度负相关，ｒ＝－０．９４３（Ｐ＜０．０５）。ＣＩＣ与ＩＬ－８呈高度正相关，相关系数ｒ＝０．８２９（Ｐ＜０．０５）。本文进一步证明了ＩＣＧＮ发病机制大多是由于ＩＣ大量形成，机体排除ＩＣ功能低下，ＩＣ沉积于肾小球，细胞因子调控功能异常，造成肾损所致。

Pathogenesis of ICGN was studied by AESSR.The experimental results indicated that the levels of serum CIC was increased significantly in model group;while CMSC was decreased markedly.The levels of sIL-2R,IL-2,IL-8,IFN and TNF were all higher in model group than those in normal group.A highly negative correlation was present between CIC and CMSC,but a highly positive correlation was present between CIC and IL-8.The results showed that CIC was precipitated in kidney and led to ICGN when CIC was greatly formed and CMSC was decreased and cytokines was disordered.