Karanjin, the furanoflavonoid reported to possess gastroprotective and anti-diabetic properties, was investigated against
experimental arthritis and its molecular signalling in
inflammation was explored in macrophages.
Karanjin was isolated from
hexane extract of Pongamia pinnata seeds and was evaluated on
arthritis markers in adjuvant induced
arthritis model (AIA) in two doses (per oral; 10 mg/kg/day and 20 mg/kg/day).
Karanjin dose dependently reduced
collagen and cartilage breakdown markers viz. urinary
hydroxyproline and
glucosamine, respectively, serum lysosomal
enzymes responsible for articular cartilage damage, and major proinflammatory
cytokine TNFα, secreted by macrophages involved in articular
inflammation and destruction.
Karanjin also prevented joint damage as evidenced from
arthritis score, radiographic and histopathological analysis. To delineate the molecular target of
Karanjin, in vitro study on LPS induced macrophages were performed at calibrated non toxic doses (4 µg/mL and 6 µg/mL).
Karanjin reduced TNFα production and also showed potent inhibitory effect on
nitric oxide and
reactive oxygen species production which is generally induced by TNFα from activated macrophages. NF-κB, the key regulator of TNFα signalling during
inflammation was significantly suppressed by
Karanjin. Our study for the first time highlights the anti-inflammatory role of
Karanjin in
experimental arthritis model as well as on macrophage signalling, thereby depicting its probable mechanism of action.