Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 15, 2004; 10(2): 238-243
Published online Jan 15, 2004. doi: 10.3748/wjg.v10.i2.238
Dynamic changes of capillarization and peri-sinusoid fibrosis in alcoholic liver diseases
Guang-Fu Xu, Xin-Yue Wang, Gui-Ling Ge, Peng-Tao Li, Xu Jia, De-Lu Tian, Liang-Duo Jiang, Jin-Xiang Yang
Guang-Fu Xu, Xin-Yue Wang, De-Lu Tian, Liang-Duo Jiang, Jin-Xiang Yang, Digestive Department of the Affiliated Dongzhimen Hospital, Beijing University of Traditional Chinese Medicine, Beijing 100700, China
Gui-Ling Ge, Central Electronic Microscope Examination Studio of Beijing University of TCM, Beijing 100029, China
Peng-Tao Li, Xu Jia, Basic Medical College of Beijing University of TCM, Beijing 100029, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Guang-Fu Xu, Digestive Department of the Affiliated Dongzhimen Hospital, Beijing University of TCM, Beijing 100700, China. guangfuxu@hotmail.com
Telephone: +86-10-84290755
Received: May 12, 2003
Revised: May 30, 2003
Accepted: June 7, 2003
Published online: January 15, 2004
Abstract

AIM: To investigate the dynamic changes of capillarization and peri-sinusoid fibrosis in an alcoholic liver disease model induced by a new method.

METHODS: Male SD rats were randomly divided into 6 groups, namely normal, 4 d, 2 w, 4 w, 9 w and 11 w groups. The animals were fed with a mixture of alcohol for designated days and then decollated, and their livers were harvested to examine the pathological changes of hepatocytes, hepatic stellate cells, sinusoidal endothelial cells, sinusoid, peri-sinusoid. The generation of three kinds of extra cellular matrix was also observed.

RESULTS: The injury of hepatocytes became severer as modeling going on. Under electronic microscope, fatty vesicles and swollen mitochondria in hepatocytes, activated hepatic stellate cells with fibrils could been seen near or around it. Fenestrae of sinusoidal endothelial cells were decreased or disappeared, sinusoidal basement was formed. Under light microscopy typical peri-sinusoid fibrosis, gridding-like fibrosis, broaden portal areas, hepatocyte’s fatty and balloon denaturation, iron sediment, dot necrosis, congregated lymphatic cells and leukocytes were observed. Type I collagen showed an increasing trend as modeling going on, slightly recovered when modeling stopped for 2 weeks. Meanwhile, type IV collagen decreased rapidly when modeling began and recovered after modeling stopped for 2 weeks. Laminin increased as soon as modeling began and did not recover when modeling stopped for 2 weeks.

CONCLUSION: The pathological changes of the model were similar to that of human ALD, but mild in degree. It had typical peri-sinusoid fibrosis, however, capillarization seemed to be instable. It may be related with the reduction of type IV collagen in the basement of sinusoid during modeling.

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