目的：探讨人肝炎慢性化过程中各型胶原沉积的规律和机制。方法：选择人体肝病材料１６３例，按正常肝、急性肝炎、慢性肝炎分为３组。用免疫组织化学方法对Ⅰ、Ⅲ、Ⅳ、Ⅴ、Ⅵ型胶原的组织分布进行分析，并研究了结蛋白（Ｄｅｓ）、α－平滑肌肌动蛋白（α－ＳＭＡ）阳性细胞与胶原分布间的关系。采用图像分析对各型胶原在肝病组织中的含量进行相对定量测定。结果：急性肝炎时，各型胶原在点灶状坏死处沉积增多。慢性肝炎时，胶原沉积的形态分布多样。各类坏死区及纤维间隔内有大量胶原沉积，并出现“架桥”现象。Ⅴ、Ⅵ型胶原随肝纤维化进展形态有所改变。坏死及炎症活动区出现较多形态似储脂细胞（ＦＳＣ）的Ｄｅｓ、α－ＳＭＡ阳性细胞。相对定量结果表明，随肝炎慢性化程度的加重，各型胶原在肝内的沉积均有上升。以Ⅰ、Ⅲ、Ⅵ型胶原上升幅度为明显。肝细胞坏死炎症明显时各型胶原的沉积均高于病变静止时。结论：进一步证实人慢性肝炎时ＦＳＣ激活增生与肝细胞的坏死和炎症反应有关，也和各型胶原产生沉积有关 Objective: To investigate the regularity and mechanism of collagen deposition in the process of chronic hepatitis. Methods: 163 cases of human liver disease were selected according to normal liver, acute hepatitis and chronic hepatitis and divided into 3 groups. The distribution of collagen type Ⅰ, Ⅲ, Ⅳ, Ⅴ and Ⅵ collagen was analyzed by immunohistochemistry and the relationship between the distribution of desmin and α-smooth muscle actin (α-SMA) . The relative quantitative determination of the content of each type of collagen in liver tissue was performed by image analysis. Results: In acute hepatitis, the deposition of various types of collagen in focal necrosis increased. Chronic hepatitis, collagen deposition of diverse forms. Various types of necrotic area and fibrous septa within a large number of collagen deposition, and the emergence of “bridging” phenomenon. Ⅴ, Ⅵ collagen with morphological changes of hepatic fibrosis has changed. Des, α-SMA positive cells appeared in necrotic and inflammatory areas with more FSC-like morphology. Relative quantitative results show that, with the degree of chronic hepatitis increased, the deposition of various types of collagen in the liver have increased. With Ⅰ, Ⅲ, Ⅵ collagen increased significantly. Hepatocyte necrosis obvious inflammation when the deposition of various types of collagen are higher than when the lesion at rest. Conclusion: It is further confirmed that FSC activation and proliferation in human chronic hepatitis are related to the necrosis and inflammatory response of hepatocytes, and also to the deposition of various types of collagen