# Hepatoprotective effects of oyster-derived bioactive compounds in alcoholic liver disease: a systematic review

**Authors:** Rui Chen, Yanan Qin, Ping Yu

PMC · DOI: 10.3389/fgstr.2026.1737942 · 2026-03-17

## TL;DR

This review examines how compounds from oysters may protect the liver in alcohol-related diseases, showing promise in animal studies but needing more human research.

## Contribution

The study is the first systematic review evaluating oyster-derived bioactives for alcoholic liver disease.

## Key findings

- Oyster compounds reduced liver enzymes and improved antioxidants in animal models of ALD.
- Inflammatory markers like TNF-α and IL-6 were lowered in preclinical studies.
- Human trial showed limited effects, highlighting the need for more clinical research.

## Abstract

Alcoholic liver disease (ALD) is a major global cause of liver-related morbidity and mortality, driven by excessive alcohol consumption and characterized by oxidative stress, inflammation, disordered lipid metabolism, and gut–liver axis dysfunction. Oyster-derived bioactive compounds have shown hepatoprotective potential in experimental settings; however, their efficacy and role in ALD management remain unclear.

To systematically evaluate and synthesize preclinical and clinical evidence on oyster-derived bioactive compounds for the prevention and treatment of ALD.

PubMed, Web of Science, and Scopus were searched for studies examining oyster-derived bioactives, including polysaccharides, peptides, protein hydrolysates, and related extracts, in alcohol-induced liver injury models. Two reviewers independently screened studies and extracted data. Risk of bias was assessed using the SYRCLE tool for animal studies and RoB 2.0 for human trials. Certainty of evidence was evaluated using the GRADE framework.

Eleven studies met the inclusion criteria, comprising ten animal studies and one randomized controlled trial. In animal models, oyster-derived interventions reduced alanine and aspartate aminotransferase levels by approximately 34-56%, increased antioxidant defenses (glutathione and superoxide dismutase increased by up to 45% and 40%, respectively), and decreased inflammatory mediators including TNF-α, IL-1β, and IL-6. Improvements in lipid metabolism and gut–liver axis markers were also reported in several studies. The single human trial demonstrated a modest reduction in γ-glutamyl transferase, with no significant changes in ALT or AST. Overall, the certainty of evidence ranged from very low to low, reflecting methodological heterogeneity, risk of bias, and limited human data.

Oyster-derived bioactives consistently demonstrate hepatoprotective effects in preclinical models of ALD through antioxidant, anti-inflammatory, metabolic, and gut-mediated mechanisms. However, the current evidence base is preliminary, and well-designed, adequately powered clinical trials are required to determine their clinical efficacy, optimal formulation, and long-term safety.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420251104584, identifier CRD420251104584.

## Linked entities

- **Diseases:** alcoholic liver disease (MONDO:0043693)

## Full-text entities

- **Genes:** GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** ALD (MESH:D008108), inflammation (MESH:D007249), disordered lipid metabolism (MESH:D052439), gut-liver axis dysfunction (MESH:D017093)
- **Chemicals:** glutathione (MESH:D005978), alanine (MESH:D000409), polysaccharides (MESH:D011134), lipid (MESH:D008055), alcohol (MESH:D000438)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13035715/full.md

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Source: https://tomesphere.com/paper/PMC13035715