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骆驼奶可调节急性酒精性肝病小鼠模型中肠道微生物组和转录组的乙醇诱导变化。

Camel milk modulates ethanol-induced changes in the gut microbiome and transcriptome in a mouse model of acute alcoholic liver disease.

机构信息

Key Laboratory of Dairy Biotechnology and Bioengineering, Ministry of Education, College of Food Science and Engineering, Inner Mongolia Agricultural University, Hohhot 010018, China.

Key Laboratory of Dairy Biotechnology and Bioengineering, Ministry of Education, College of Food Science and Engineering, Inner Mongolia Agricultural University, Hohhot 010018, China; Camel Research Institute of Inner Mongolia, Alashan 737300, China.

出版信息

J Dairy Sci. 2020 May;103(5):3937-3949. doi: 10.3168/jds.2019-17247. Epub 2020 Mar 12.

Abstract

Morbidity and mortality as a result of liver disease are major problems around the world, especially from alcoholic liver disease (ALD), which is characterized by hepatic inflammation and intestinal microbial imbalance. In this study, we investigated the hepatoprotective effects of camel milk (CM) in a mouse model of acute ALD and the underlying mechanism at the gut microbiota and transcriptome level. Male Institute of Cancer Research mice (n = 24; Beijing Weitong Lihua Experimental Animal Technology Co. Ltd., China) were divided into 3 groups: normal diet (NC); normal diet, then ethanol (ET); and normal diet and camel milk (CM), then ethanol (ET+CM). Analysis of serum biochemical indexes and histology revealed a reduction in hepatic inflammation in the ET+CM group. Sequencing of 16S rRNA showed that CM modulated the microbial communities, with an increased proportion of Lactobacillus and reduced Bacteroides, Alistipes, and Rikenellaceae RC9 gut group. Comparative hepatic transcriptome analysis revealed 315 differentially expressed genes (DEG) in the ET+CM and ET groups (150 upregulated and 165 downregulated). Enrichment analysis revealed that CM downregulated the expression of inflammation-related (ILB and CXCL1) genes in the IL-17 and tumor necrosis factor (TNF-α) pathways. We conclude that CM modulates liver inflammation and alleviates the intestinal microbial disorder caused by acute alcohol injury, indicating the potential of dietary CM in protection against alcohol-induced liver injury.

摘要

肝脏疾病导致的发病率和死亡率是全球范围内的主要问题,尤其是酒精性肝病(ALD),其特征为肝炎症和肠道微生物失衡。在这项研究中,我们在急性 ALD 的小鼠模型中研究了骆驼奶(CM)的保肝作用及其在肠道微生物组和转录组水平的潜在机制。雄性癌症研究所小鼠(n=24;北京维通利华实验动物技术有限公司,中国)分为 3 组:正常饮食(NC);正常饮食,然后乙醇(ET);正常饮食和骆驼奶(CM),然后乙醇(ET+CM)。血清生化指标和组织学分析表明,ET+CM 组肝炎症减少。16S rRNA 测序显示 CM 调节了微生物群落,乳杆菌的比例增加,而拟杆菌、双歧杆菌和理研菌科 RC9 肠道群的比例减少。比较肝转录组分析显示,ET+CM 和 ET 组有 315 个差异表达基因(DEG)(150 个上调,165 个下调)。富集分析表明,CM 下调了 IL-17 和肿瘤坏死因子(TNF-α)通路中与炎症相关的(ILB 和 CXCL1)基因的表达。我们得出结论,CM 调节肝炎症并减轻急性酒精损伤引起的肠道微生物失调,表明饮食 CM 具有预防酒精性肝损伤的潜力。

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