Urginea indica has been used in the traditional system of medicine to treat various inflammatory diseases.
Present study investigates the effects of aqueous and ethanolic extracts of U. indica on joint inflammation using different models of acute and chronic inflammation.
FCA-induced arthritic rat model, a model of chronic joint inflammation, was used to evaluate the anti-arthritic effects of plant extracts (500 mg/kg, each extract). Macroscopic arthritic scoring, digital water plethysmometery, and histopathological evaluation (H & E staining) were performed to measure the severity of arthritis. Acute inflammatory models like, carrageenan-, histamine- and serotonin-induced paw edema models were used to evaluate effects of U. indica, and supported by xylene-induced ear edema model.
Both extracts significantly inhibited arthritic development, paw edema, bone erosion, pannus formation, and infiltration of inflammatory cells. Treatment with U. indica extracts resulted in almost normalization of altered counts of white blood cells (WBCs), platelets, and red blood cells (RBCs), along with Hb content. Both extracts were found safe in terms of hepatotoxicity and nephrotoxicity as determined by non-significant difference of alanine aminotransferase (ALT), aspartate transaminase (AST), urea, and creatinine levels among all groups. U. indica significantly attenuated carrageenan-induced paw edema. There are several mechanisms involved in the attenuation of carrageenan-induced paw edema; inhibition of autacoids is one of those important mechanisms. The autacoid inhibition was confirmed by reduction of histamine- and serotonin-induced paw edema found in plant extract treated groups. Suppression of xylene-induced ear edema by plant extract further validated the suggested mechanism of autacoid inhibition. GC-MS analysis showed the presence of isopropyl palmitate in the highest quantity (26.852%).
This study validated the folkloric uses of U. indica and showed that plant possessed anti-arthritic and anti-inflammatory properties which might be ascribed to inhibition of autacoids.