Betanin Mitigates Inflammation and Ankle Joint Damage by Subduing the MAPK/NF-κB Pathway in Arthritis Triggered by Type II Collagen in Rats

Rheumatoid Arthritis (RA), a chronic inflammatory autoimmune illness, is characterized by synovitis, progressive joint damage, and bone erosion. Even though the potent drugs available contain biologics, several patients fail to react to them or cause hostile effects. Betanin (BTN), the betacyanin present in the red beetroot, has antioxidant, antiinflammatory, and apoptotic properties. In this study, we assessed the anti-inflammatory and apoptotic effect of BTN on collagen-induced arthritis (CIA). The rats were arbitrarily separated into four sets: Normal, CIA, CIA+BTN (25 mg/kg bw), and CIA+BTN (50 mg/kg bw). The hematological, biochemical markers, cytokines, inflammatory enzymes, histopathology of the ankle joint, and protein expression of inflammatory and apoptotic proteins were studied. Inflammatory enzymes, histopathological variations, cytokines generation, and joint inflammation were strongly alleviated, and apoptosis was augmented by BTN in a concentrationdependent manner. Bcl-2 and MAPK/NF-κB proteins were reduced, while the caspase-3, caspase- 9, and Bax were intensified. The anti-rheumatic action of BTN was correlated to the attenuation of the MAPK/NF-κB pathway, which suppresses cytokine production, inflammation, and reduced cartilage impairments. These outcomes recommend that BTN can be employed as a strong healing alternative for RA management.