【摘要】 目的 :从黏膜免疫及炎症相关细胞因子的角度探讨脾虚痹证的发病机理。方法 :选用Ⅱ型胶原诱导的小鼠关节炎 (CIA)作为痹证模型 ;复合大黄泻下加饥饱失常造成实验动物脾虚 ;以酶联免疫吸附法测定小鼠血清中肿瘤坏死因子 α、白细胞介素 6、干扰素 γ、白细胞介素 10等细胞因子含量 ,以免疫组织化学方法测定小肠组织中CD4、CD8、分泌型IgA含量 ,并对肠道集合淋巴结(PEYER SPATCH ,PP结 )计数。结果 :脾虚组、脾虚痹证组肠道PP结数量明显减少 ,CIA组变化不明显。CIA组及脾虚痹证组血清中TNF α、IL 6含量显著升高 ,CIA组及脾虚痹证组血清中IFN γ含量显著升高 ;与空白对照组比较 ,CIA组、脾虚痹证组CD4、CD8阳性细胞均明显减少 ,而以脾虚痹证组CD8阳性细胞减少更为明显 ;正常组、CIA组SIgA阳性细胞较多 ,脾虚组、脾虚痹证组则明显减少。结论 :脾虚时可能是通过下调机体黏膜免疫功能 ,相对上调全身免疫应答而加重CIA发病更多还原

【Abstract】 Aims:to explore the pathogenesis of Bi-syndrome(arthritis) superimposed on spleen deficiency by investigating the changes of mucosal immune functions and inflammation-related cytokines.Methods:Arthristis was induced by type Ⅱ collagen (CIA) superimposed on spleen deficiency in DBA mice.Enzyme-linked immunoadsorbent assay (ELISA) was employed to detect the levels of tumor necrosis factor-α,interleukin-6,interferon-γ and interleukin-10 in serum,and immunohistochemistry methods was used to assay CD\-4,CD\-8 and secretory immunoglobulin A in the tissues of small intestine.The numbers of intestinal PEYER’S PATCH(PP) was calculated.Results:the number of intestinal PP apparently reduced in mice with spleen deficiency and in mice with spleen-deficiency-CIA,while there was no significant changes in CIA mice.The leovels of TNF-α\,IL-6 in serum increased significantly in CIA mice and in spleen-deficiency-CIA mice.The content of IFN-γ in serum highly increased while IL-10 decreased in CIA and spleen-deficiency-CIA mice.Compared to that in controlled mice,CD4+ and CD8+ Cells reduced in CIA and spleen-deficiency-CIA mice.SigA positive cells were more in normal and CIA mice,while it reduced apparently in spleen-deficiency and spleen-deficiency-CIA mice.Conclusion:spleen-deficiency may exacerbate the CIA by down-regulate mucosal immunofunctions and relatively up-regulate general immune responses.更多还原