NF-κB and Nrf2 pathways contribute to the protective effect of Licochalcone A on dextran sulphate sodium-induced ulcerative colitis in mice.

Licochalcone A (Lico A) is a characteristic chalcone isolated from licorice root which is widely recognized in traditional Chinese medicine for the ability of anti-inflammatory, antioxidant, anti-parasitic and anti-cancer. The present study was aimed to investigate the effect of Lico A on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) in a mouse model which was induced by administration of 3% DSS in drinking water. Mice were then treated with Lico A (20, 40 and 80 mg/kg, p.o.) or 0.9% saline (20 ml/kg, p.o.) for 17 days. The results showed that treatment with Lico A significantly reduced the colon length, histological damage scores, and colonic myeloperoxidase (MPO) activity in a dose-dependent manner as compared to the UC control group. Besides, Lico A significantly decreased the oxidative stress and pro-inflammatory cytokines, downregulated nuclear transcription factor kappa B (NF-κB) pathway and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Collectively, Lico A is effective in alleviating DSS-induced colitis in mice and the mechanism is associated with its inhibition of NF-κB-regulated pro-inflammatory signaling and activation of Nrf2-regulated cytoprotective protein expression.