title: Dietary vitamin E and quercetin modulate inflammatory responses of collagen-induced arthritis in mice.
abstract: Rheumatoid arthritis (RA) is characterized by chronic inflammation of the synovial joints. This study investigated whether or not a diet deficient in vitamin E is a possible risk factor in the development of RA and evaluated the efficacy of antioxidant supplementation. Male DBA/1J mice were maintained on either a control diet (C) or a vitamin E-depleted (-VE) diet for 4 weeks before arthritis induction. The mice in the control group were subdivided into the control group (C/C), the 0.05% alpha-tocopherol-supplemented group (C/+VE), and the 0.5% quercetin-supplemented group (C/+Q). The vitamin E-depleted group was subdivided into the -VE group (-VE/-VE), the 0.05% alpha-tocopherol-supplemented group (-VE/+VE), and the 0.5% quercetin-supplemented group (-VE/+Q) (in total, six groups, 27 mice per group). The mice were maintained on the experimental diets for 9 weeks. Study results indicate that the -VE/-VE group showed higher joint tissue tumor necrosis factor-alpha and interleukin-1beta mRNA expressions, whereas alpha-tocopherol or quercetin supplementation reduced tissue cytokine mRNA levels to values comparable to those of the C/C group. The mice fed the -VE/-VE diet exhibited higher levels of circulating macrophage chemoattractant protein 1, nitric oxide, and prostaglandin E(2) compared to those in other groups. Supplementation with alpha-tocopherol or quercetin in mice fed -VE diet decreased these markers similar to those of the mice in the C/C group. No supplementation effect was observed, however, in the mice fed with the control diet prior to RA induction. These results suggest that dietary deficiency of vitamin E increases inflammatory responses and that antioxidants successfully suppress the inflammatory responses. However, significant clinical improvement may require longer observation.
authors.affiliation: Department of Food and Nutrition, Sookmyung Women's University, Seoul, Republic of Korea.
authors.forename: Eun-Jin
authors.initials: EJ
authors.lastname: Choi
authors.forename: Sang-Cheol
authors.initials: SC
authors.lastname: Bae
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
authors.forename: Jeehee
authors.initials: J
authors.lastname: Youn
authors.forename: Mi-Kyung
authors.initials: MK
authors.lastname: Sung
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001169:Arthritis, Experimental / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D003094:Collagen; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004032:Diet; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D011794:Quercetin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D012307:Risk Factors; D014811:Vitamin E Deficiency / Q000150:complications*; D024502:alpha-Tocopherol / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; D012333:RNA, Messenger; D003094:Collagen; D011794:Quercetin; D024502:alpha-Tocopherol