Effect of alcoholic extract of Entada pursaetha DC on monosodium iodoacetate-induced osteoarthritis pain in rats

Osteoarthritis (OA) is a chronic joint disease characterized by progressive cartilage degeneration, synovial inflammation, subchondral bone sclerosis, and osteophyte formation1. A complex network of cytokines and proteolytic enzymes leads to degradation of the extracellular matrix (ECM) proteins of cartilage such as type II collagen (CII), proteoglycans and hyaluronic acid2. Although studies have confirmed the efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) and anti-cycloxygenase-2 (COX-2) as symptomatic treatments for OA, these drugs have not proven to positively affect the natural course of OA in humans3. In this context, diacerein has been shown as an attractive candidate4. Monosodium iodoacetate (MIA)-induced OA model used in this study mimics severe and acute OA pain which is similar with human OA 5. The MIA-induced OA model is highly reproducible with predictable pain behaviour responses. Entada pursaetha, a large gigantic woody climbing shrub (liana) among legumes is widely distributed in tropical Africa, India, China, Philippines, Guam and Northern Australia6. In India, it is found in damp forest of Bengal, Bihar and Odisha, in forest region of Eastern and Western Ghat and hilly forest tract of northern district of Bengal and Deccan7. Mainly seeds, leaves and stem or stem bark of E. pursaetha are used for different medicinal purposes. Antibacterial, antiviral, analgesic, anti-inflammatory and hypoglycaemic activities of plant extracts have been studied earlier8. Free radical scavenging activity of leaf extract9 and anti-inflammatory and hepatoprotective activity of seed extract of E. pursaetha have also been reported10,11. But no study has been done on its anti-arthritic or anti-osteoarthritis activity. In the present study, we investigated whether ethanolic extract of E. pursaetha (EPE) stem would suppress OA pain and its progression by examining behavioural pain parameters and histopathological changes elicited in MIA-induced experimental OA rat model.