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To investigate the protective effect and potential molecular mechanism of fucoidan on alcoholic liver injury.
A mouse model of alcoholic liver disease (ALD) was established using 50% (V/V) alcohol, and then administered with 300 mg/kg mb of fucoidan. Liver histomorphological changes were compared in the control, ALD and fucoidan intervention groups, and the levels of serum aminotransferase, serum lipids, and inflammatory factors, the proportion of T helper (Th) cells including Th1, Th2 and Th17, and the expression levels of autophagy-related proteins and microtubule-associated protein 1 light chain 3 beta (LC3B) were detected to explore the mechanism by which fucoidan can improve alcoholic liver injury.
Fucoidan could improve the pathological changes of liver tissue, reduce the levels of serum alanine (aminotransferase (ALT) and aspartate aminotransferase (AST)) and blood lipids (triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and total bile acid (TBA)) (P < 0.05), and decrease the levels of serum inflammatory factors (TNF-α, IL-1β and IL-6) and the proportion of Th1, Th2 and Th17 (P < 0.05). Meanwhile, it could down-regulate the expression of autophagy-related protein p62, mammalian target of rapamycin complex 1 (mTORC1) and ribosomal protein 70S6 kinase (p70S6K) (P < 0.05), promote the nuclear translocation of transcription factor EB (TFEB) (P < 0.05), and up-regulate the expression of LC3B Ⅱ protein and LC3B fluorescent protein (P < 0.05).
Fucoidan can alleviate lipotoxicity and inflammatory injury in the liver of ALD mice, and its mechanism may be related to the activation of autophagy.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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