The effect of ganoderic acid a application on arthritis parameters in experimentally induced rheumatoid arthritis model mice

INTRODUCTION AND AIM: Rheumatoid arthritis (RA) is an autoimmune disease characterized by the destruction of articular cartilage and bone tissue. Currently, various agents are used in the treatment of RA. The effect of Ganoderic Acid A (GAA), found in the content of Ganoderma Lucidum fungus, which has been traditionally used in Traditional Chinese Medicine and plays significant roles, is not well understood in experimental RA. This study aims to investigate the effect of GAA on RA in mice with experimentally induced RA models. MATERIALS AND METHODS: On the 1st day, the Control (K) group was administered physiological saline (SF), the Acetic Acid (AA) group was administered acetic acid; the Experiment (D) group, Low GAA (DGAA), and High dose GAA (YGAA) groups were administered collagen emulsion intra-articularly (i.a), while completed Freund's adjuvant (CFA) was administered subcutaneously (s.c). On the 22nd day, the procedures were repeated, and on this day, incomplete Freund's adjuvant was administered s.c to the D, DGAA, and YGAA groups instead of CFA. From the 22nd day for 9 days, the K, AA, and D groups received SF; the DGAA and YGAA groups were administered GAA orally at the determined dose. The therapeutic effect of GAA in the experimental RA model was evaluated using arthritis parameters and histopathological assessment methods. RESULTS: In comparison to the D group, the YGAA group significantly reduced arthritis scores (p≤0,05), caused a decrease in knee joint temperature compared to the GAA groups (p≤0,05), led to a decrease in knee joint circumference (p≤0,05), reduced parameters related to pain (p≤0,05), and improved histopathological parameters (p≤0,05). CONCLUSION: It was observed that GAA slowed down the decrease in body weight, reduced arthritis scores, reduced edema and inflammation, contributed to analgesic effects, improved locomotor activity, and reduced damage to joint cartilage and bone structure caused by RA.