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目的和方法：利用复合因子（以四氯化碳为主要因素）致大鼠肝纤维化模型，探讨肠源性内毒素血症在肝纤维化发生发展中的作用。结果：（１）血浆内毒素水平在肝纤维化过程中逐渐升高，且与肝胶原蛋白含量变化正相关；（２）血浆ＴＮＦα测定及ＴＮＦα免疫组化定位研究，均表明ＴＮＦα参与了内毒素介导的肝纤维化过程；（３）肝组织Ⅰ、Ⅲ型胶原酶活性均在肝纤维化早期增高，晚期呈下降趋势。超微结构观察显示贮脂细胞在此过程中发生表型转化，提示贮脂细胞功能状态与内毒素在肝纤维化过程中的作用密切相关。结论：肠源性内毒素血症在肝纤维化发生发展中起重要作用
PURPOSE AND METHODS: The hepatic fibrosis model induced by compound factor (carbon tetrachloride is the main factor) was used to explore the role of intestinal endotoxemia in the development of hepatic fibrosis. Results: (1) Plasma endotoxin levels increased gradually during hepatic fibrosis and positively correlated with changes of hepatic collagen content. (2) Measurement of plasma TNFα and immunohistochemical localization of TNFα showed that TNFα was involved in endotoxin Mediated liver fibrosis process; (3) liver tissue collagenase type Ⅰ, Ⅲ were increased in the early stage of liver fibrosis, a downward trend in the late. Ultrastructural observation revealed that phenotypic transformation of the storage fat cells occurred during this process, suggesting that the functional status of the storage fat cells is closely related to the role of endotoxin in hepatic fibrosis. Conclusion: Intestinal endotoxemia plays an important role in the development of hepatic fibrosis