Dietary supplementation of krill oil attenuates inflammation and oxidative stress in experimental ulcerative colitis in rats

Abstract

Objective. To evaluate the effects of krill oil (KO) on inflammation and redox status in dextran sulfate sodium (DSS)-induced colitis in rats. Materials and methods . Thirty male Wistar rats were divided into three groups: Control, DSS, and DSS + KO 5% in a 4-week diet study. Colitis was induced by 5% DSS in the drinking water the last week of the experiment. Weight and disease activity index (DAI), colon length, histological combined score (HCS), colon levels of selected cytokines and prostaglandins, markers of protein oxidative damage, fatty acid profile, and expression of selected genes were measured. Results. Rats in the DSS group increased their DAI and HCS compared with healthy controls. The colon length was significantly preserved after KO diet. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β were elevated in the DSS group compared with controls. Cytokines and HCS were nonsignificantly lower in the KO versus the DSS group. Prostaglandin (PG)E₃ increased significantly in the KO versus the other groups. Peroxisome proliferator-activated receptor (PPAR)-γ expression was nonsignificantly increased while PPAR-γ coactivator 1α (Pparg1α) expression increased significantly after KO. The levels of protein oxidation markers decreased significantly. Conclusions . KO showed protective potential against DSS colitis based on the preservation of colon length, reduction of oxidative markers and the consistent beneficial changes of HCS, cytokine, and (PG)E₃ levels, as well as PPAR-γ and Pparg1α expression compared with DSS alone. These findings indicate an anti-inflammatory and a protein antioxidant effect of KO.

Key Words::

• colitis
• diet therapy
• inflammatory bowel diseases
• omega-3 fatty acids

Acknowledgements

Aker Biomarine is thanked for providing krill oil used in this experiment. Ingeborg Kvivik, Kari Espedal and Marita Hanasand are thanked for their substantial efforts during the cytokine analyses, and Torunn Eide for the analyses of prostaglandins. We thank Eline Milde, Kari Williams, Liv Kristine Øysæd, and Randi Sandvik for excellent technical assistance. Sources of support: The research was supported by the Board of Nutrition Programmes (University of Bergen, Western Norway Regional Health Authority and the Institute of Marine Research), and partly from the Nordic Centre of Excellence – MitoHealth. Work carried out at the Department of Experimental Medicine was supported by grants from the Spanish Ministry of Science and Innovation (BFU2009-11879/BFI), the Autonomous Government of Catalonia (2009SGR735), and the Spanish Ministry of Health (PI081843, PI011532) to MPO and RP. Supported also by COST B-35 action. DC holds a fellowship from the Spanish Ministry of Health (FI0800707).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.