COUNTRY: Republic of Korea
CONDUCTED BY: College of Biomedical & Health Science, Department of Life Science, Konkuk University, Chungju, Republic of Korea; Functional Food Center, KIST Gangneung Institute, Gangwon, Republic of Korea
PUBLISHED ON: The Journal of Nutritional Biochemistry
Inflammatory bowel disease (IBD) is an inflammatory disorder caused by hyperactivation of effector immune cells that produce high levels of proinflammatory cytokines. The aims of our study were to determine whether orally-administered Blueberry extract could attenuate or prevent the development of experimental colitis in mice and to elucidate the mechanism of action. Female Balb/C mice (n=7) were randomized into groups differing in treatment conditions (prevention and treatment) and dose of Blueberry extract (50 mg/kg body weight). Acute ulcerative colitis was induced by oral administration of 3% dextran sodium sulfate (DSS) for 7 days in drinking water. Colonic mucosal injury was assessed by clinical, macroscopic, biochemical, and histopathological examinations.
Blueberry extract significantly decreased disease activity index and improved the macroscopic and histological score of colons when compared to the colitis group (P<0.05). BE markedly attenuated myeloperoxidase accumulation (colitis group 54.97±2.78 while treatment group 30.78±1.33 nmol/mg) and malondialdehyde in colon and prostaglandin E2 level in serum while increasing the levels of superoxide dismutase and catalase (colitis group 11.94±1.16 and Blueberry extract treatment group 16.49±0.39 U/ml) compared with the colitis group (P<0.05). mRNA levels of the COX-2, IFN-γ, IL-1β, and iNOS cytokines were determined by RT-PCR.
Immunohistochemical analysis showed that Blueberry extract attenuates the expression of COX-2 and IL-1β in colonic tissue. Moreover, Blueberry extract reduced the nuclear translocation of NF-κB by immunofluorescence analysis.
Thus the anti-inflammatory effect of Blueberry extract at colorectal sites is a result of a number of mechanisms: antioxidation, downregulation of the expression of inflammatory mediators, and inhibition of the nuclear translocation of NF-κB.