Berberine reduce inflammation in RA rats through MCP1/CCR2 pathway

Abstract

AbstractRheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovitis and systemic inflammation, leading to joint damage and functional disability. Current treatment modalities, although effective, may pose significant side effects. In this study, we investigated the anti-inflammatory properties of berberine, a natural isoquinoline alkaloid, and its potential role in ameliorating RA-associated inflammation in rats through modulation of the monocyte chemoattractant protein-1 (MCP1)/chemokine receptor 2 (CCR2) pathway. A collagen-induced arthritis (CIA) rat model was employed to mimic RA pathophysiology. Rats were treated with berberine or RS504393 for 30 days. Joint swelling, arthritis score, histopathology used to evaluate disease progression and the extent of inflammation. Immunohistochemistry and WB were used to detect the mechanism of action of berberine. Our results demonstrated that berberine treatment significantly reduced joint swelling, and inflammatory factors in CIA rats. Furthermore, berberine downregulated MCP1 and CCR2 expression, implicating the involvement of the MCP1/CCR2 signaling pathway in attenuating RA-associated inflammation. Taken together, our findings suggest that berberine may represent a promising therapeutic candidate for the management of RA and highlight the potential of targeting the MCP1/CCR2 pathway to mitigate inflammation in autoimmune diseases.