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

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.

Medicinal herbs and their metabolites with biological potential to protect and combat liver toxicity and its disorders: A review

“…On the other hand, the ethanol-induced histopathological alterations, lipid metabolism disorders, and oxidative damage were mitigated by the fucoidan pretreatment, leading to the restoration of normal levels of proteins related to mitophagy and mitochondrial dynamics. These proteins include mitochondrial E3 ubiquitin ligase 1 (Mul1), mitofusin 2 (Mfn2), and dynamin-related protein 1 (Drp1) [ 252 , 253 ] (see Fig. 4 ).…”

Fucoidan derived from Sargassum pallidum alleviates metabolism disorders associated with improvement of cardiac injury and oxidative stress in diabetic mice

“…The db/db and db/m groups were treated with physiological saline intragastrically for 8 weeks, while the mice in the db/m + SP‐Fuc and db/db + SP‐Fuc groups were administered intragastrically with SP‐Fuc at 200 mg/(kg/d) dissolved with physiological saline. The selection of a dosage of 200 mg/(kg/d) of SP‐Fuc was based on previous research indicating that fucoidan derived from brown algae has the potential to treat metabolic disorders (Liu et al, 2022a; Xue et al, 2021), as well as on our own preliminary experiments.…”

Long Noncoding RNA MIAT Regulates Hyperosmotic Stress-Induced Corneal Epithelial Cell Injury via Inhibiting the Caspase-1-Dependent Pyroptosis and Apoptosis in Dry Eye Disease

“…Cells were lysed in radioimmunoprecipitation assay (RIPA, Solarbio, Beijing, China) lysis buffer containing phenylmethanesulfonyl fluoride (PMSF, 100:1; Solarbio) for 2 h, and then were centrifuged at 4°C, 16,000 g for 10 min. The total protein content in each sample was detected using a Pierce™ Rapid Gold BCA (bicinchoninic acid) Protein Assay Kit (Thermo Scientific, Shanghai, China), 19 and mixed with SDS sample buffer (1:1) and boiled for 10 min at 95°C. Samples (equivalent to 30 μg total protein) were separated by 10–12% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred onto a polyvinylidene difluoride (PVDF) membrane.…”