Date Published: March 18, 2019
Publisher: Public Library of Science
Author(s): Tien-Chien Pan, Yu-Hsin Tsai, Wen-Chi Chen, Yueh-Ling Hsieh, Chuen-Mao Yang.
Articular cartilage damage related to irreversible physical disability affects most patients with chronic rheumatoid arthritis (RA). Strategies targeting the preservation of cartilage function are needed. Laser acupuncture (LA) can be an emerging alternative therapy for RA; however, its molecular mechanism underlying the beneficial effect on cartilage has not been elucidated. This study aimed to examine the potential chondroprotective effects of LA on extracellular matrix (ECM) macromolecules and proinflammatory cytokines in the articular cartilage of adjuvant-induced arthritis (AIA) rats and explore its related mechanisms.
Monoarthritis was induced in adult male Sprague–Dawley rats (250–300 g) via intraarticular injection of complete Freund’s adjuvant (CFA) into the tibiotarsal joint. Animals were treated with LA at BL60 and KI3 acupoints three days after CFA administration with a 780 nm GaAlAs laser at 15 J/cm2 daily for ten days. The main outcome measures including paw circumference, paw withdrawal threshold, histopathology and immunoassays of tumor necrosis factor-α (TNF-α), collagen type II (CoII), cartilage oligomeric matrix protein (COMP) were analyzed.
LA significantly reduced ankle edema and inflammation-induced hyperalgesia in AIA rats (P < 0.05). Moreover, the TNF-α levels were significantly decreased while CoII, COMP and proteoglycans proteins were significantly enhanced following LA stimulation of the AIA cartilage compared to those treated with sham-LA (P < 0.05). LA attenuates cartilage degradation in AIA rat by suppressing TNF-α activation and up-regulating ECM macromolecules, suggesting LA might be of potential clinical interest in RA treatment.
Rheumatoid arthritis (RA) is characterized by persistent synovial inflammation and hyperplasia, which eventually lead to articular cartilage destruction and disability . Articular cartilage damage is related to irreversible physical disability of RA and special attention should be given to therapeutic interference with cartilage damage . However, most studies on the treatment strategies of RA focused on reducing synovial hyperplasia and inflammatory cell infiltration, with less attention being paid to the delay in the pathogenesis of cartilage damage.
Our study results demonstrated the chondroprotective effects of LA in reducing proinflammatory cytokine TNF-α, and enhancing the protein levels of proteoglycans, CoII and COMP in the superficial and transitional zones of the cartilage, indicating improvement of joint inflammation and cartilage ECM anabolic bioactivity in AIA rats. LA is also a promising treatment modality to elevate the nociceptive withdrawal threshold and reduce edema. Therefore, LA appears to promote cartilage repair in inflammation-induced cartilage destruction, probably due to its efficiency in modulating most of the main factors involved in the pathogenesis of this disease.
To our knowledge, this study is the first to present outcomes of LA on protection against cartilage pathohistological degradation in rats with AIA-induced cartilage damage. Our study’s results demonstrate LA intervention may be effective in delay of cartilage degradation and cartilage repair by promoting CoII, proteoglycans and COMP expressions in ECM, reducing inflammatory cell infiltration and TNF-α in cartilage. Whether catabolic processes of ECM can also be modulated by LA for reducing the cartilage destruction in RA deserves further intensive research.