腹膜粘连动态过程的细胞机制研究

The research of the cellular pathophysiology mechanism in the process of peritoneal adhesion

目的动态观察创伤、感染时的腹膜粘连,探讨腹膜粘连相关细胞的病理生理机制。方法健康Wister大鼠240只,分为创伤粘连组、创伤感染组、正常组,每组80只。分别于1、3、7、14 d观察粘连情况、HE染色、测定血清t-PA、PAI、FDP含量。分离培养巨噬细胞、间皮细胞、成纤维细胞,分别经LPS、TGF、TNF处理后,测定TNF、PAI、t-PA及间皮细胞、成纤维细胞的增殖率。结果感染、炎症、间皮细胞损伤引起巨噬细胞活化,分泌炎症细胞因子及PAI;成纤维细胞在LPS、TGF-β及细胞因子的刺激下,增殖活跃;局部的炎症反应抑制间皮细胞的修复和t-PA的分泌。结论间皮细胞损伤、巨噬细胞活化、纤维蛋白渗出、成纤维细胞过度增殖是粘连形成的病理生理基础,并存在着腹腔内感染、炎症反应、损伤纤维蛋白渗出、纤维蛋白基质形成成纤维细胞迁移、机化的时间顺序。

Objective To investigate the cellular pathophysiology mechanism of peritoneal adhesion induced by trauma or infection. Methods Two hundred and forty healthy Wistar rats were randomly divided into three groups （trauma group, trauma ＋ infection group, and control group）. The status of adhesion was observed by HE staining, and the serum levels of TNF, IL-6, PAI and t-PA were simultaneously measured on 1,3,7 and 14 days. Macrophages, mesothelial cells and fibroblasts were isolated and cultured. Biomarkers including TNF, IL-6, PAI and t-PA were measured and the proliferating activity of the above cells was analyzed after pretreatment with LPS,TGF or TNF. Results Macrophage was activated after infection, inflammation or mesothelial cell injury and secreted inflammatory factors and PAL Pretreatment with LPS,TGF- or cytokine promoted the proliferating activity of fibroblast while local inflammation suppressed mesothelial cells repair and secretory activity. Conclusions Mesothelial cell injury,macrophage activation, fiber exudation and fibroblast proliferation all contributed to the formation of peritoneal adhesion. The whole process may include intra-abdominal infection, inflammation, fiber exudation, matrix formation as well as fibroblast proliferation,migration and fibro- SiS.