Mechanism of the Antioxidant Action of Antarctic Krill Oil in Mice with Ulcerative Colitis Induced by Dextran Sulfate Sodium

To explore the antioxidant effect and underlying mechanism of Antarctic krill oil (AKO) in mice suffering from dextran sulfate sodium (DSS)-induced ulcerative colitis (UC).

BALB/c mice were randomly divided into four groups: normal, UC model, low-dose AKO (L-AKO, 0.25 g/(kg m_b·d)) and high-dose (H-AKO, 0.5 g/(kg m_b·d)) AKO treatments.Mice were induced to develop UC by adding 3.5% DSS to their drinking water for one week.Colon tissues were collected after the mice were euthanized to observe histological changes by hematoxylin-eosin (H&E) staining, and the expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), lipopolysaccharides (LPS), and diamine oxidase (DAO) in colon tissues were detected.Quantitative polymerase chain reaction (qPCR) and Western blot were used to further determine theexpression of genes and key proteins related to the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in the colon.

H-AKO treatment could not only attenuate colon injury caused by DSS intervention, but also significantly increase the expression of antioxidant enzyme genes (P < 0.05), and reduce the levels of inflammatory factors and intestinal permeability indicators (IL-6, TNF-α, LPS and DAO) (P < 0.05) in colon tissues.qPCR results showed that H-AKO increased the gene expression of Nrf2 as well as GSH-Px, SOD and HO-1.Western blot results showed that AKO treatment activated the Nrf2 signaling pathway by increasing Nrf2 protein and decreasing Keap1 protein expression.

AKO can exert antioxidant protection in UC mice through activating the expression of genes and proteins related to the Nrf2 signaling pathway, enhancing the expression of antioxidant enzymes, thereby reducing oxidative stress injury, suppressing inflammatory response, and restoring intestinal barrier structure and function.