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Dietary alpha lipoic acid supplementation prevents synovial inflammation and bone destruction in collagen-induced arthritic mice
Authors:Young-Sool Hah  Mi Jeong Sung  Hye Song Lim  Jin-Su Jun  Yong-Genu Jeong  Hyun-Ok Kim  Junghwan Kim  Haeng Jeon Hur  Munkhtugs Davaatseren  Dae Young Kwon  Sang-Il Lee
Affiliation:1. Clinical Research Institute, Gyeongsang National University Hospital and Department of Internal Medicine and Institute of Health Science, Gyeongsang National University College of Medicine, #92, Chilam-dong, Jinju, Gyeongnam, 660-702, Republic of Korea
2. Research Division for Emerging Innovative Technology, Korea Food Research Institute, #516 Baekhyun-dong, Bundang-ku, Sungnam, Gyeonggi-do, 463-746, Republic of Korea
3. Food Biotechnology, University of Science & Technology, Daejeon, Republic of Korea
Abstract:Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by chronic inflammation and joint destruction. In this study, we investigated whether dietary supplementation with alpha lipoic acid (ALA) suppresses collagen-induced arthritis (CIA) in mice. Mice were randomly divided into three groups: (1) a control CIA group was fed a normal diet, (2) a CIA group was fed a 0.1% ALA diet (average ALA intake of 160?mg/kg/day), and (3) a CIA group was fed a 0.5% ALA diet (average ALA intake of 800?mg/kg/day). The ALA-fed mice showed a decreased incidence and severity of arthritis compared to the normal diet group. Radiographic findings revealed a dramatic decrease in bone destruction, and histological findings showed extensively suppressed pathological changes in the ALA-fed mice. The ALA-fed mice exhibited inhibited generation of tartrate resistant acid phosphatase (TRAP)-positive osteoclasts in vivo. Additionally, ALA-fed mice reduced production of various proinflammatory cytokines and the soluble receptor activator of NF-??B ligand (sRANKL) in the joint tissues and the sera. In conclusion, dietary supplementation with ALA attenuated inflammatory responses and bone destruction in CIA mice.
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