Anti-hyperalgesic and anti-inflammatory effects of long term calcium administration during adjuvant-induced arthritis in rats

Introduction: Inflammation and edema Symptoms are physiological responses to triggers induced by different mediators such as cytokines. Rheumatoid arthritis is the most common form of arthritis which is characterized by chronic inflammation of the synovial membrane, severe and debilitating pain, and progressive cartilage injury. It is clear that cytokines are involved in different stages of inflammation by inducing pro-inflammatory effects; TNF-? is a cytokine involved in the pathogenesis of rheumatoid arthritis. In this study, we attempted to investigate the role of the prescription of calcium to reduce inflammatory edema and serum TNF-? levels during different stages of arthritic inflammation induced by Complete Freund Adjuvant (CFA) injection in males Wistar rats. Methods: In this Applicable-Fundamental study, we used male Wistar rats and adjuvant arthritis was created by once the subcutaneous injection of CFA in the right hind paw of animals on day zero in experimental groups. Various doses of calcium were prepared and injected within 21 days of the study. Hyperalgesia and paw volume changes were assessed by radiant heat and plethysmometer over several days, respectively. The serum levels of TNF-? were studied by ELISA standard kit of rats during various phases and were measured according to the kit. Results: The results indicated dose-related effects of long-term calcium administration on edema, hyperalgesia, and serum TNF-? level reduction. Daily treatment with an effective dose of calcium (5 mg/kg) in the AA+ Ca group significantly decreased paw edema, hyperalgesia, and serum TNF-? level in comparison to AA and AA+ Vehicle groups on days 7, 14, and 21 of the study. Conclusions: Findings of this study showed; long-term administration of calcium in the proper dosage can act as an anti-inflammatory agent and pain modulator during adjuvant-induced arthritis. A part of those effects may be conducted by decreasing serum TNF-? levels.