摘要
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。
Purpose To explore the role and mechanism of the deposition of the 5 types of collagen during the continuation of human hepatitis. Methods A total of 163 human liver specimens were divided into 3 groups: normal liver, acute hepatitis, chronic hepatitis. The five collagen types(Ⅰ,Ⅲ,Ⅳ,Ⅴ and Ⅵ) were studied by immunohistochemical techniques and computerized image procession. The relationship between desmin (Des), α smooth muscle actin (α SMA) positive cells and collagens deposition were also studied. Results The five collagen types were increased in acute hepatitis. In chronic hepatitis, the bulk of collagens were found to deposit in piecemeal or focal necrosis and fibrotic septa. There were many Des and α SMA positive cells whose morphology were much like fat storing cell (FSC) and abundantly deposited in the site of necrosis. Relative quantification indicated that with the progression of the chronic hepatitis, all the five collagen types elevated, especially type Ⅰ,Ⅲ,Ⅵ collagen. Conclusion The results above were further proved in morphology that the activation and proliferation of FSC were related to hepatocellular necrosis and inflammation, also to collagen depositions.
出处
《临床与实验病理学杂志》
CAS
CSCD
1998年第4期315-318,I043,共5页
Chinese Journal of Clinical and Experimental Pathology
基金
国家自然科学基金
关键词
肝炎
病毒性肝炎
胶原
结蛋白
肌动蛋白类
hepatitis,viral,human
collagen
desmin
actins
immunohistochemistry
