Therapeutic Effect and Underlying Mechanism of Blue Mussel (Mytilus galloprovincialis) Oil on Adjuvant-Induced Rheumatoid Arthritis in Rats

TL;DR

This study shows that blue mussel oil can reduce inflammation and joint damage in rats with rheumatoid arthritis, possibly by targeting key inflammatory pathways.

Contribution

The study identifies blue mussel oil as a potential therapeutic agent for rheumatoid arthritis and explores its mechanism of action.

Findings

Blue mussel oil reduced paw swelling and inflammatory markers in rats with rheumatoid arthritis.

Blue mussel oil suppressed the NF-κB and JAK2/STAT3 signaling pathways in synovial tissue.

Blue mussel oil showed slightly better effects than green-lipped mussel oil and krill oil in alleviating arthritis symptoms.

Abstract

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovitis. The prevalence of RA is estimated to be 0.5–1% worldwide. Methods: This work investigated the therapeutic effects and underlying mechanisms of blue mussel (Mytilus galloprovincialis) oil (BMO) on RA in rats, using green-lipped mussel oil (GMO) and Antarctic krill oil (KO) as controls. Results: The results suggested that BMO, GMO, and KO all alleviated paw swelling in rats and reduced serum levels of rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibody, and pro-inflammatory cytokines such as TNF-α and IL-17. Histopathological assessment further revealed that BMO, GMO, and KO prevented synovial fibroplasia, mitigated inflammatory cell infiltration, and improved cartilage damage in ankle joints. Overall, BMO exhibited slightly superior alleviating effects compared with GMO and KO. Plasma lipidomics analysis revealed that the lipid metabolites altered by BMO showed significant correlations with RA-related indicators, particularly pro-inflammatory cytokines. Functional enrichment analysis suggested the involvement of inflammation-related pathways, particularly the NF-κB signaling pathway. Further validation demonstrated that BMO effectively suppressed the production of inflammatory cytokines (TNF-α, IL-17) and the expression of NF-κB p65, JAK2, and STAT3 proteins in synovial tissue. And IL-17 production in footpad tissues is closely associated with CD3-positive T cells. Similar effects were also observed for GMO and KO. Conclusions: Collectively, BMO might ameliorate RA by inhibiting NF-κB and JAK2/STAT3 signaling pathways.

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