Effect of fucoidan on ethanol-induced liver injury and steatosis in mice and the underlying mechanism

  • Meilan Xue Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
  • Hui Liang The Institute of Human Nutrition, College of Public Health, Qingdao University of Medicine, 308# Ningxia Road, Qingdao, 266071, PR China
  • Zhitong Zhou Food Science Department, University of Guelph, Guelph, Ontario, Canada
  • Ying Liu Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
  • Xinjia He Oncology Department, The Affiliated Hospital of Qingdao University, Qingdao, PR China
  • Zheng Zhang Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
  • Ting Sun Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
  • Jia Yang Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
  • Yimin Qin State Key Laboratory of Bioactive Seaweed Substances, Qingdao Brightmoon Seaweed Group Co., Ltd., Qingdao, China
  • Kunpeng Qin Department of Biochemistry and Molecular Biology, Basic Medical College, Qingdao University of Medicine, Qingdao, PR China
Keywords: fucoidan; ethanol-induced liver injury; AMPKα1/SIRT1 pathway; gut microbiota-bile acid-liver axis

Abstract

Background: Alcoholic liver disease is caused as a result of chronic alcohol consumption. In this study, we used an alcoholic liver injury mouse model to investigate the effect of fucoidan on ethanol-induced liver injury and steatosis and the underlying mechanisms.

Methods: All mice were randomly divided into four groups: 1) control group, 2) model group, 3) diammonium glycyrrhizinate treatment group (200 mg/kg body weight), and 4) fucoidan treatment group (300 mg/kg body weight). Administration of ethanol for 8 weeks induced liver injury and steatosis in mice.

Results: Fucoidan treatment decreased serum alanine aminotransferase activity, serum total cholesterol levels, and hepatic triglyceride levels, and improved the morphology of hepatic cells. Fucoidan treatment upregulated the expression of AMPKα1, SIRT1, and PGC-1α and inhibited the expression of ChREBP and HNF-1α. The levels of hepatic IL-6 and IL-18 were significantly decreased in the fucoidan group. Further, the levels of cytochrome P450-2E1 (CYP2E1), glucose-regulated protein (GRP) 78, and 3-nitrotyrosine (3-NT) in hepatic tissues were reduced in the fucoidan group as compared to the model group. Fucoidan significantly reversed the reduction of ileac Farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15) levels induced by alcohol- feeding and reduced CYP7A1 (cholesterol 7α-hydroxylase) expression and total bile acid levels in the liver tissue. In addition, fucoidan regulated the structure of gut flora, with increased abundance of Prevotella and decreased abundance of Paraprevotella and Romboutsia as detected by 16S rDNA high-throughput sequencing.

Conclusion: Fucoidan inhibited alcohol-induced steatosis and disorders of bile acid metabolism in mice through the AMPKα1/SIRT1 pathway and the gut microbiota–bile acid–liver axis and protected against alcohol- induced liver injury in vivo.

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Published
2021-04-20
How to Cite
Xue M., Liang H., Zhou Z., Liu Y., He X., Zhang Z., Sun T., Yang J., Qin Y., & Qin K. (2021). Effect of fucoidan on ethanol-induced liver injury and steatosis in mice and the underlying mechanism. Food & Nutrition Research, 65. https://doi.org/10.29219/fnr.v65.5384
Section
Original Articles