Journal Article

Curcumin alleviates rheumatoid arthritis-induced inflammation and synovial hyperplasia by targeting mTOR pathway in rats

Dai, Qiaoding, Zhou, Di, Xu, Liping, Song, Xinwei

2018

نظرة عامة

Rheumatoid arthritis (RA) is a chronic, progressive autoimmune disease characterized by aggressive and symmetric polyarthritis. Mammalian target of rapamycin (mTOR) was reported to be a new target for RA therapy and its inhibitor rapamycin can significantly reduce the invasive force of fibroblast-like synoviocytes. Here, we determined the effect of curcumin to alleviate inflammation and synovial hyperplasia for the therapy of RA. Collagen-induced arthritis (CIA) was developed in Wistar rats and used as a model resembling RA in humans. Rats were treated with curcumin (200 mg/kg) and the mTOR inhibitor rapamycin (2.5 mg/kg) daily for 3 weeks. Effects of the treatment on local joint, peripheral blood, and synovial hyperplasia in the pathogenesis of CIA were analyzed. Curcumin and rapamycin significantly inhibited the redness and swelling of ankles and joints in RA rats. Curcumin inhibited the CIA-induced mTOR pathway and the RA-induced infiltration of inflammatory cells into the synovium. Curcumin and rapamycin treatment inhibited the increased levels of proinflammatory cytokines including IL-1β, TNF-α, MMP-1, and MMP-3 in CIA rats. Our findings show that curcumin alleviates CIA-induced inflammation, synovial hyperplasia, and the other main features involved in the pathogenesis of CIA via the mTOR pathway. These results provide evidence for the anti-arthritic properties of curcumin and corroborate its potential use for the treatment of RA.

• الناشر: Dove Medical Press Limited,Taylor & Francis Ltd,Dove Medical Press
• موضوع: Animals / Anti-Inflammatory Agents - pharmacology / Antirheumatic Agents - pharmacology / Apoptosis / Arthritis / Arthritis, Experimental - chemically induced / Arthritis, Experimental - enzymology / Arthritis, Experimental - pathology / Arthritis, Experimental - prevention & control / Atherosclerosis / Autoimmune diseases / Autophagy / Cell adhesion & migration / Cell cycle / Cell growth / CIA / Collagen / Collagen Type II / Curcumin / Curcumin - pharmacology / Cytokines / EDTA / Fibroblasts / Government agencies / Hyperplasia / IL-1β / Induced infiltration / Infiltration / Inflammation / Inflammation Mediators - metabolism / Inhibitors / Interleukin-1beta - metabolism / Interstitial collagenase / Joint diseases / Laboratory animals / Male / Matrix metalloproteinase / Matrix Metalloproteinase 1 - metabolism / Matrix Metalloproteinase 3 - metabolism / Medical research / Metabolism / mTOR / Multiple sclerosis / Original Research / Pathogenesis / Peripheral blood / Polyarthritis / Protein Kinase Inhibitors - pharmacology / Proto-Oncogene Proteins c-akt - metabolism / Rapamycin / Rats, Wistar / Rheumatoid arthritis / Rheumatoid factor / Rodents / Signal Transduction - drug effects / Sirolimus - pharmacology / Synovial Membrane - drug effects / Synovial Membrane - enzymology / Synovial Membrane - pathology / Synoviocytes / Synovitis - chemically induced / Synovitis - enzymology / Synovitis - pathology / Synovitis - prevention & control / Synovium / Therapy / TOR protein / TOR Serine-Threonine Kinases - antagonists & inhibitors / TOR Serine-Threonine Kinases - metabolism / Tumor Necrosis Factor-alpha - metabolism / Tumor necrosis factor-α