title: Dietary alpha lipoic acid supplementation prevents synovial inflammation and bone destruction in collagen-induced arthritic mice.
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-κB ligand (sRANKL) in the joint tissues and the sera. In conclusion, dietary supplementation with ALA attenuated inflammatory responses and bone destruction in CIA mice.
authors.affiliation: 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.
authors.forename: Young-Sool
authors.initials: YS
authors.lastname: Hah
authors.forename: Mi Jeong
authors.initials: MJ
authors.lastname: Sung
authors.forename: Hye Song
authors.initials: HS
authors.lastname: Lim
authors.forename: Jin-Su
authors.initials: JS
authors.lastname: Jun
authors.forename: Yong-Genu
authors.initials: YG
authors.lastname: Jeong
authors.forename: Hyun-Ok
authors.initials: HO
authors.lastname: Kim
authors.forename: Junghwan
authors.initials: J
authors.lastname: Kim
authors.forename: Haeng Jeon
authors.initials: HJ
authors.lastname: Hur
authors.forename: Munkhtugs
authors.initials: M
authors.lastname: Davaatseren
authors.forename: Dae Young
authors.initials: DY
authors.lastname: Kwon
authors.forename: Sang-Il
authors.initials: SI
authors.lastname: Lee
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001169:Arthritis, Experimental / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D001172:Arthritis, Rheumatoid / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology; D001862:Bone Resorption / Q000000981:diagnostic imaging / Q000517:prevention & control*; D016207:Cytokines / Q000096:biosynthesis; D019587:Dietary Supplements; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D010010:Osteoclasts / Q000201:enzymology; D053245:RANK Ligand / Q000096:biosynthesis; D011859:Radiography; D012720:Severity of Illness Index; D013585:Synovitis / Q000517:prevention & control*; D000071681:Tartrate-Resistant Acid Phosphatase; D008063:Thioctic Acid / Q000627:therapeutic use*
chemical_list: D018501:Antirheumatic Agents; D016207:Cytokines; D007527:Isoenzymes; D053245:RANK Ligand; C505689:Tnfsf11 protein, mouse; D008063:Thioctic Acid; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase