摘要
为探讨脂肪肝与肝纤维化的关系及其机制，以高脂饮食和（或）酒精诱发Ｗｉｓ－ｔａｒ大鼠脂肪肝模型，观察造模３个月和６个月时肝脏病理学变化，分析造模６个月时肝内甘油三酯（ＴＧ）、丙二醛（ＭＤＡ）含量与羟脯氨酸（Ｈｙｐ）含量及α－平滑肌肌动蛋白（α－ＳＭＡ）阳性细胞数间的相关性。结果：与低脂饮食组相比，高脂饮食组ＴＧ显著升高，但ＭＤＡ和Ｈｙｐ及α－ＳＭＡ阳性细胞数基本正常；低脂饮食酒精组ＴＧ、ＭＤＡ、Ｈｙｐ和α－ＳＭＡ阳性细胞数均显著增多，高脂饮食酒精组以上改变更加明显，各指标与其他３组相比差异均有显著性；各组ＴＧ含量与α－ＳＭＡ阳性细胞数均不相关，ＴＧ与Ｈｙｐ仅在低脂饮食酒精组呈正相关，而ＭＤＡ与Ｈｙｐ和α－ＳＭＡ细胞数间在低脂饮食酒精组和高脂饮食酒精组均呈正相关。结果提示肝内脂肪本身与贮脂细胞激活和肝纤维化形成间并无直接关系，但其可通过增强肝脏脂质过氧化反应促进肝纤维化的发生和发展。
To explore the correlation between hepatic fat and fibrosis and the possible causative mechanism. 40 Wistar rats were randomized into 4 groups i.e. low fat diet (group Ⅰ), high fat diet (group Ⅱ), low fat diet plus ethanol (group Ⅲ), high fat diet plus ethanol (group Ⅳ). Rats were sacrificed at 3 and 6 months after experiment. Triglyceride (TG), malonaldehyde (MDA) and hydroproline (Hyp) content in the liver were measured with biochemical analysis. The degree of steatosis and fibrosis and the amount of αsmooth muscle actin (αSMA) positive cells in the liver were determined by HE, van Giesson and immunohistochemical ABC stain, respectively. Results: Steatosis was observed in most of the group Ⅱ, Ⅲ, Ⅳ animals including those sacrificed at 3 months after experiment, but increased amount of αSMA positive cells and hepatic fibrosis was only shown in group Ⅲ and Ⅳ. As compared with group Ⅰ, hepatic TG content was increased significantly in the group Ⅱ, Ⅲ, Ⅳ animals, and hepatic MDA and Hyp content were increased significantly in the group Ⅲ, Ⅳ animals. Moreover, changes of these biochemical and histological indexes in group Ⅳ were the most outstanding. There was no significant correlation between hepatic TG content and amount of αSMA positive cells in group Ⅱ, Ⅲ, Ⅳ and no correlation between hepatic TG and Hyp content in group Ⅱ, Ⅳ, and there was significant correlation between hepatic MDA content and Hyp content and the number of αSMA positive cells in group Ⅲ, Ⅳ. Conclusions: there is no direct relationship between steatosis and initiation of lipocyte activation and resulting fibrogenesis, but hepatic fat per se may promote the initiation and development of hepatic fibrosis induced by the injurious factors of increasing lipid peroxidation.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1997年第12期808-811,共4页
Chinese Journal of Internal Medicine
基金
国家自然科学基金
