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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Activation of the endotoxin/toll-like receptor 4 pathway: the way to go from nonalcoholic steatohepatitis up to hepatocellular carcinoma.
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Activation of the endotoxin/toll-like receptor 4 pathway: the way to go from nonalcoholic steatohepatitis up to hepatocellular carcinoma.

机译:内毒素/ toll样受体4途径的激活:从非酒精性脂肪性肝炎到肝细胞癌的途径。

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摘要

We read with great interest the article by Yu et al.1 on the role of gut-derived endotoxin in hepatocarcinogenesis. In particular, the authors demonstrated that increased levels of endotoxemia observed in an experimental animal model of chemically induced hepatocarcinogenesis, were protective against liver cell apoptosis and seemed to promote the development of hepatocellular carcinoma (HCC). In fact, Yu et al. found that treatment with antibiotics partially protected rats from diethylnitrosamine-induced hepatocarcinogenesis, which reduced the number of tumors and their maximum size. In addition, the animals treated with antibiotics showed decreased plasma levels of lipopolysaccharide (LPS) and hepatic levels of tumor necrosis factor alpha and interleukin-6 messenger RNA. Interestingly, diethylnitrosamine-induced HCC was reduced in toll-like receptor 4 (TLR4) mutant mice, and they displayed a lower incidence of tumors and a smaller maximum tumor size associated with reduced infiltration of macrophages with respect to the control animals.
机译:我们非常感兴趣地阅读了Yu等人1的文章,即肠源性内毒素在肝癌发生中的作用。特别是,作者证明,在化学诱导的肝癌发生的实验动物模型中观察到的内毒素血症水平升高,对肝细胞凋亡具有保护作用,并且似乎促进了肝细胞癌(HCC)的发展。实际上,Yu等。发现用抗生素治疗可以部分保护大鼠免受二乙基亚硝胺诱导的肝癌发生,从而减少了肿瘤的数量及其最大尺寸。此外,用抗生素治疗的动物血浆脂多糖(LPS)水平降低,肝脏肿瘤坏死因子α和白介素6信使RNA降低。有趣的是,二乙基亚硝胺诱导的HCC在收费样受体4(TLR4)突变小鼠中减少,并且相对于对照动物,它们显示出较低的肿瘤发生率和较小的最大肿瘤尺寸,与巨噬细胞浸润减少相关。

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