Selegiline modulates inflammatory indicators in RAW 264.7 macrophages and LPS-aggravated CFA-induced rheumatoid arthritis in rats

Introduction and aim. Rheumatoid arthritis (RA) causes pain, inflammation, and deformities in numerous joints. Monoamine oxidase B (MOA-B) inhibitor selegiline exhibits anti-inflammatory characteristics and has the propensity to scavenge free rad icals. Therefore, the aim of this research comprises of assessing the effect of selegiline on proinflammatory cytokines in RAW 264.7 macrophages as well as its capacity to improve various arthritic parameters in rats with lipopolysaccharide (LPS) acceler ated complete Freund’s adjuvant (CFA) induced RA. Material and methods. In RAW 264.7 cells (lipopolysaccharide accelerated), nitric oxide (NO), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), and prostaglandin E2 (PGE2 ) were determined after treat ment with selegiline. Different arthritic parameters were analyzed after administration of selegiline in LPS accelerated CFA-in duced arthritis in rats. Results. LPS escalates NO, TNF-α, IL-6, iNOS, and PGE2 quantities in the RAW 264.7 cells, which was minimized by selegiline at 100 µg/mL and 150 µg/mL respectively. In rats, CFA induction causes a decrease in body weight, elevation of paw volume, splenic index, and arthritic index, which are further accelerated by LPS. 20 mg/kg of selegiline managed all these arthritic pa rameters effectively, including TNF-α, IL-6, and a few other biochemical parameters. Conclusion. Selegiline may be beneficial in RA extenuating joint and cartilage damage, and modulating inflammatory responses.