Preventive Effect of Lycopene in Dextran Sulfate Sodium-Induced Ulcerative Colitis Mice through the Regulation of TLR4/TRIF/NF-κB Signaling Pathway and Tight Junctions

The preventive effect and molecular mechanism of lycopene (LP) in dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice were evaluated. Compared to the DSS group, the LP prevention groups not only significantly inhibited the DSS-induced weight loss, decreased the disease activity index (DAI) score, increased the colon length, and improved inflammation in the colon but also significantly increased the levels of superoxide dismutase (SOD),catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) in the colon and reduced inflammatory cytokine, myeloperoxidase (MPO), and malondialdehyde (MDA) levels. Notably, when compared to the DSS group, the protein expression levels of TLR4, TRIF, and p-NF-kappa B p65 in the mice colon tissue were downregulated and those of tight junction-related proteins were upregulated in the LP + DSS group, with the most significant effect observed in the 10 mg/kg LP + DSS group. These results confirmed that the upregulation of tight junction related protein expression after blocking the TLR4/TRIF/NF-kappa B signaling pathway may be one of the mechanisms through which LP prevents UC.

Automated summary

The study demonstrated the preventive effect of lycopene in dextran sulfate sodium-induced ulcerative colitis in mice by increasing anti-oxidant levels, reducing inflammation, and upregulating tight junction-related proteins through modulation of the TLR4/TRIF/NF-κB signaling pathway.