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Dynamic changes of capillarization and peri-sinusoid fibrosis in alcoholic liver diseases

机译:酒精性肝病中毛细血管化和窦窦周围纤维化的动态变化

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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.
机译:目的:探讨一种新方法诱发的酒精性肝病模型中毛细血管化和窦窦周纤维化的动态变化。方法:雄性SD大鼠随机分为6组,即正常组,4 d,2 w,4 w,9 w和11 w组。在指定的日子里给动物喂食酒精混合物,然后脱颈,收集它们的肝脏以检查肝细胞,肝星状细胞,正弦内皮细胞,正弦,正弦周围的病理变化。还观察到了三种细胞外基质的产生。结果:随着建模的进行,肝细胞的损伤变得更加严重。在电子显微镜下,可在肝细胞附近或周围看到脂肪囊泡和肝细胞线粒体肿胀,并激活了带有原纤维的肝星状细胞。窦状内皮细胞的窗孔减少或消失,形成了窦状基底。在光学显微镜下观察到典型的正弦周围纤维化,网格样纤维化,门脉区域变宽,肝细胞的脂肪和球囊变性,铁沉积物,小点坏死,聚集的淋巴细胞和白细胞。随着建模的进行,Ⅰ型胶原蛋白呈增加趋势,当建模停止2周时,胶原蛋白逐渐恢复。同时,Ⅳ型胶原在开始建模时迅速减少,在停止建模两周后恢复。层粘连蛋白一开始建模就增加,而在模型停止2周后却没有恢复。结论:模型的病理变化与人ALD相似,但程度较轻。它具有典型的正弦周围纤维化,但是毛细血管化似乎不稳定。建模过程中可能与窦道基底中Ⅳ型胶原的减少有关。

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