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首页> 外文期刊>Yonsei Medical Journal >S100A4 Gene is Crucial for Methionine-Choline-Deficient Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice
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S100A4 Gene is Crucial for Methionine-Choline-Deficient Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice

机译：S100A4基因对于蛋氨酸-胆碱缺乏饮食引起的小鼠非酒精性脂肪肝疾病至关重要

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Purpose pTo explore the influence of S100 calcium binding protein A4 (S100A4) knockout (KO) on methionine-choline-deficient (MCD) diet-induced non-alcoholic fatty liver disease (NAFLD) in mice. Materials and Methods pS100A4 KO mice (n=20) and their wild-type (WT) counterparts (n=20) were randomly divided into KO/MCD, Ko/methionine-choline-sufficient (MCS), WT/MCD, and WT/MCS groups. After 8 weeks of feeding, blood lipid and liver function-related indexes were measured. HE, Oil Red O, and Masson stainings were used to observe the changes of liver histopathology. Additionally, expressions of S100A4 and proinflammatory and profibrogenic cytokines were detected by qRT-PCR and Western blot, while hepatocyte apoptosis was revealed by TUNEL staining. Results pSerum levels of aminotransferase, aspartate aminotransferase, triglyceride, and total cholesterol in mice were increased after 8-week MCD feeding, and hepatocytes performed varying balloon-like changes with increased inflammatory cell infiltration and collagen fibers; however, these effects were improved in mice of KO/MCD group. Meanwhile, total NAFLD activity scores and fibrosis were lower compared to WT+MCD group. Compared to WT/MCS group, S100A4 expression in liver tissue of WT/MCD group was enhanced. The expression of proinflammatory (TNF-α, IL-1β, IL-6) and profibrogenic cytokines (TGF-β1, COL1A1, α-SMA) in MCD-induced NAFLD mice were increased, as well as apoptotic index (AI). For MCD group, the expressions of proinflammatory and profibrogenic cytokines and AI in KO mice were lower than those of WT mice. Conclusion pS100A4 was detected to be upregulated in NAFLD, while S100A4 KO alleviated liver fibrosis and inflammation, in addition to inhibiting hepatocyte apoptosis.
机译：目的>探讨S100钙结合蛋白A4（S100A4）敲除（KO）对蛋氨酸-胆碱缺乏症（MCD）饮食引起的小鼠非酒精性脂肪性肝病（NAFLD）的影响。材料与方法将S100A4 KO小鼠（n = 20）和其野生型（WT）小鼠（n = 20）随机分为KO / MCD，Ko /蛋氨酸-胆碱充足（MCS），WT / MCD和WT / MCS组。喂养8周后，测量血脂和肝功能相关指标。 HE，油红O和Masson染色用于观察肝脏组织病理学的变化。另外，通过qRT-PCR和Western印迹检测S100A4的表达以及促炎和促纤维化细胞因子的表达，而通过TUNEL染色揭示肝细胞凋亡。结果喂食MCD 8周后，小鼠血清中的氨基转移酶，天冬氨酸氨基转移酶，甘油三酸酯和总胆固醇水平升高，并且肝细胞随着炎症性细胞浸润和胶原纤维的增加而发生不同的气球样变化。然而，这些作用在KO / MCD组小鼠中得到改善。同时，总的NAFLD活性评分和纤维化低于WT + MCD组。与WT / MCS组相比，WT / MCD组肝组织中S100A4表达增强。 MCD诱导的NAFLD小鼠中促炎性（TNF-α，IL-1β，IL-6）和促纤维化细胞因子（TGF-β1，COL1A1，α-SMA）的表达增加，并且细胞凋亡指数（AI）升高。对于MCD组，KO小鼠中促炎和纤维原细胞因子和AI的表达低于WT小鼠。结论在NAFLD中检测到> S100A4被上调，而S100A4 KO除了抑制肝细胞凋亡外，还减轻了肝纤维化和炎症。

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