Anti-inflammatory activity and mechanisms of a lipid extract from hard-shelled mussel (Mytilus coruscus) in mice with dextran sulphate sodium-induced colitis. (May 2016)

• Record Type: Journal Article
• Authors: Wang, Fenglei; Fu, Yuanqing; Cai, Wenwen; Sinclair, Andrew J.; Li, Duo
• Is Part Of: Journal of functional foods. Volume 23(2016)
• Page Start: 389
• Page End: 399
• Publication Date: 2016-05
• Subjects: Hard-shelled mussel -- Lipid extract -- Salicylazosulphapyridine -- Colitis -- Anti-inflammatory -- TLR-4/NF-κB pathway; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2016.03.002
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: Effect of HMLE on DSS-induced colitis in mice was assessed. HMLE regulated the production of NO, MPO, TNF-α, IL-1β, IL-6, and IL-10. The mechanism might rely on the modulation of the TLR-4/NF-κB pathway. Overall effect was comparable with standard anti-inflammatory drug SASP. Abstract: The anti-inflammatory effect of a lipid extract from hard-shelled mussel (HMLE) on dextran sulphate sodium (DSS)-induced colitis in mice was investigated. Salicylazosulphapyridine (SASP) and different doses of HMLE were administered by gastric gavage. HMLE significantly attenuated DSS-induced colitis disease activity index scores, tissue damage, splenic enlargement and colon myeloperoxidase accumulation. In addition, HMLE improved colon oxidative stress and production and expression of anti-inflammatory cytokine, interleukin (IL)-10, while HMLE inhibited the abnormal productions and mRNA expressions of pro-inflammatory cytokines, namely tumour necrosis factor-α, IL-1β, and IL-6, as well as the expression of key molecules in the toll-like receptor (TLR)-4/nuclear factor (NF)-κB signalling pathway. These findings suggest that HMLE has an anti-inflammatory effect on DSS-induced colitis, equivalent to that of SASP, and this effect might be related to the regulation of inflammatory mediators and key molecules in the TLR-4/NF-κB pathway.