Alleviation of Antarctic krill oil on dextran sulfate sodium exposure induced chronic ulcerative colitis and depressive-like behavior

The present study evaluated the regulatory effects and potential mechanisms of Antarctic krill oil (KO) on chronic colitis and associated depressive-like behaviors. The mechanism suggested that KO could inhibit intestinal-brain inflammation, increase 5-hydroxytryptamine (5-HT) concentration and postsynaptic density protein 95 (PSD95) and brain-derived neurotrophic factor (BDNF) expression, protect the integrity of intestinal and blood–brain barriers, maintain gut flora balance, and alleviate colitis and associated depressive-like behaviors. • Antarctic krill oil modulated the chronic ulcerative colitis (UC) and its concomitant depressive-like behavior. • Antarctic krill oil alleviated the brain inflammation by inhibiting the NLRP3 inflammatory pathway. • Antarctic krill oil maintained the integrity of the gut-brain barrier by increasing the expression of tight junction proteins. • Antarctic krill oil augmented the concentration of 5-hydroxytryptamine (5-HT) and the expression of postsynaptic density protein 95 (PSD95) and brain-derived neurotrophic factor (BDNF) to enhance the neuronal excitation. • Antarctic krill oil regulated the equilibrium of the intestinal flora by promoting the growth of beneficial microorganisms and inhibiting the proliferation of harmful bacteria. Substantial evidence indicate that Antarctic krill oil (KO) is an effective method for alleviating acute ulcerative colitis (UC). Nevertheless, UC is a chronic disease, and the chronic colitis model is more conducive to simulating its pathological characteristics. The objective of this study was to establish a chronic UC model in C57BL/6 mice and identify the regulatory consequences and feasible mechanisms of KO on chronic UC and its associated depressive-like behaviors. The results showed that KO alleviated the pathological features of UC and depression-like behavior. Further mechanisms suggested that KO significantly suppressed gut-brain inflammation, increased the concentration of 5-hydroxytryptamine (5-HT) and the expression of postsynaptic density protein 95 (PSD95) and brain-derived neurotrophic factor (BDNF), protected the integrity of the gut barrier and blood–brain barrier. Moreover, KO maintained the equilibrium of the intestinal flora. The findings suggested that KO may be a promising approach for alleviating UC and its concomitant psychiatric disorders.