Xu Guang-Fu, Wang Xin-Yue, Ge Gui-Ling, Li Peng-Tao, Jia Xu, Tian De-Lu, Jiang Liang-Duo, Yang Jin-Xiang
Digestive Department of the Affiliated Dongzhimen Hospital, Beijing University of Traditional Chinese Medicine, Beijing 100700, China.
World J Gastroenterol. 2004 Jan 15;10(2):238-43. doi: 10.3748/wjg.v10.i2.238.
To investigate the dynamic changes of capillarization and peri-sinusoid fibrosis in an alcoholic liver disease model induced by a new method.
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.
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.
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.
采用新方法诱导酒精性肝病模型，研究其毛细血管化和窦周纤维化的动态变化。
将雄性SD大鼠随机分为6组，即正常组、4天组、2周组、4周组、9周组和11周组。给予动物指定天数的酒精混合液喂养，然后断头处死，取肝脏检查肝细胞、肝星状细胞、窦状内皮细胞、肝血窦、窦周的病理变化。同时观察三种细胞外基质的生成情况。
随着建模时间延长，肝细胞损伤加重。电镜下可见肝细胞内有脂肪空泡和肿胀的线粒体，肝星状细胞活化，其周围可见纤维。窦状内皮细胞窗孔减少或消失，形成窦状基底膜。光镜下可见典型的窦周纤维化、网格状纤维化、门静脉区增宽、肝细胞脂肪变性和气球样变性、铁沉积、点状坏死、淋巴细胞和白细胞聚集。Ⅰ型胶原随着建模时间延长呈上升趋势，建模停止2周后略有恢复。同时，Ⅳ型胶原在建模开始时迅速下降，建模停止2周后恢复。层粘连蛋白在建模开始时即升高，建模停止2周后未恢复。
该模型的病理变化与人酒精性肝病相似，但程度较轻。有典型的窦周纤维化，然而，毛细血管化似乎不稳定。这可能与建模过程中窦状基底膜中Ⅳ型胶原减少有关。
