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Coenzyme Q10 Ameliorates Pain and Cartilage Degradation in a Rat Model of Osteoarthritis by Regulating Nitric Oxide and Inflammatory Cytokines
Authors:Jennifer Lee  Yeon Sik Hong  Jeong Hee Jeong  Eun Ji Yang  Joo Yeon Jhun  Mi Kyoung Park  Young Ok Jung  Jun Ki Min  Ho Youn Kim  Sung Hwan Park  Mi-La Cho
Institution:1. Division of Rheumatology Department of Internal Medicine The Catholic University of Korea, Seoul, Korea.; 2. Rheumatism Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.; 3. Division of Rheumatology, Department of Internal Medicine, Hallym University Kang Nam Sacred Heart Hospital, Seoul, Korea.; 4. Conversant Research Consortium in Immunologic disease, College of Medicine, The Catholic University of Korea, Seoul, Korea.; University of Szeged, Hungary,
Abstract:

Objective

To investigate the effect of CoenzymeQ10 (CoQ10) on pain severity and cartilage degeneration in an experimental model of rat osteoarthritis (OA).

Materials and Methods

OA was induced in rats by intra-articular injection of monosodium iodoacetate (MIA) to the knee. Oral administration of CoQ10 was initiated on day 4 after MIA injection. Pain severity was assessed by measuring secondary tactile allodynia using the von Frey assessment test. The degree of cartilage degradation was determined by measuring cartilage thickness and the amount of proteoglycan. The mankin scoring system was also used. Expressions of matrix metalloproteinase-13 (MMP-13), interleukin-1β (IL-1β), IL-6, IL-15, inducible nitric oxide synthase (iNOS), nitrotyrosine and receptor for advanced glycation end products (RAGE) were analyzed using immunohistochemistry.

Results

Treatment with CoQ10 demonstrated an antinociceptive effect in the OA animal model. The reduction in secondary tactile allodynia was shown by an increased pain withdrawal latency and pain withdrawal threshold. CoQ10 also attenuated cartilage degeneration in the osteoarthritic joints. MMP-13, IL-1β, IL-6, IL-15, iNOS, nitrotyrosine and RAGE expressions were upregulated in OA joints and significantly reduced with CoQ10 treatment.

Conclusion

CoQ10 exerts a therapeutic effect on OA via pain suppression and cartilage degeneration by inhibiting inflammatory mediators, which play a vital role in OA pathogenesis.
Keywords:
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