Preventive and therapeutic effects of blueberry (Vaccinium corymbosum) extract against DSS-induced ulcerative colitis by regulation of antioxidant and inflammatory mediators |
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| Affiliation: | 1. College of Biomedical & Health Science, Department of Life Science, Konkuk University, Chungju, 380-701, Republic of Korea;2. Functional Food Center, KIST Gangneung Institute, 290, Daejeon-dong, Gangneung, Gangwon, 210-340, Republic of Korea;1. Pharmacology Department, Faculty of Medicine, Tanta University, Postal No. 31527, El-Gish Street, Tanta, Egypt;2. Histology Department, Faculty of Medicine, Tanta University, Postal No. 31527, El-Gish Street, Tanta, Egypt;1. State Key Laboratory of Natural Medicine, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, Nanjing 210009, China;2. Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China;2. Internal Medicine, International University of Health and Welfare, Atami Hospital, Atami, Japan;1. University of Lisbon, Faculty of Pharmacy and Research Institute for Medicines and Pharmaceutical Sciences (iMed.UL), Av. Prof. Gama Pinto, 1649-003 Lisboa, Portugal;2. Disease & Stress Biology Group, LEAF, Instituto Superior de Agronomia, Universidade de Lisboa, 1349-017 Lisbon, Portugal;3. University of Coimbra, Faculty of Medicine and Instituto Português de Oncologia, Pólo Ciências da Saúde, Celas, 3000-354 Coimbra;4. ITQB, Estação Agronómica Nacional, Av. da República, 2780-157 Oeiras, Portugal;5. IBET, Avenida da República, Quinta-do-Marquês, Estação Agronómica Nacional, 2780-157 Oeiras, Portugal |
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| Abstract: | 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 (BE) 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 BE (50 mg/kg body weight). Acute ulcerative colitis was induced by oral administration of 3% dextran sodium sulfate for 7 days in drinking water. Colonic mucosal injury was assessed by clinical, macroscopic, biochemical and histopathological examinations. BE significantly decreased disease activity index and improved the macroscopic and histological score of colons when compared to the colitis group (P<.05). BE markedly attenuated myeloperoxidase accumulation (colitis group 54.97±2.78 nmol/mg, 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 U/ml, BE treatment group 16.49±0.39 U/ml) compared with the colitis group (P<.05). mRNA levels of the cyclooxygenase (COX)-2, interferon-γ, interleukin (IL)-1β and inducible nitric oxide synthase cytokines were determined by reverse transcriptase polymerase chain reaction. Immunohistochemical analysis showed that BE attenuates the expression of COX-2 and IL-1β in colonic tissue. Moreover, BE reduced the nuclear translocation of nuclear transcription factor kappa B (NF-κB) by immunofluorescence analysis. Thus, the anti-inflammatory effect of BE at colorectal sites is a result of a number of mechanisms: antioxidation, down-regulation of the expression of inflammatory mediators and inhibition of the nuclear translocation of NF-κB. |
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