Pharmacological Effect of Kaurenoic Acid in MSU-induced Animal Model of Gout

Abstract

This study investigated the potential of kaurenoic acid (KA) in a gout model caused by monosodium urate (MSU) crystals. It was discovered that KA reduced gouty inflammation and reversed the structural, histological, and biochemical changes brought on by the MSU crystals. In this study, paw edema, joint thickness, and the frequency and duration of acute gout flare-ups were all considerably decreased by the administration of KA. Additionally, the treatment groups' behavioral parameters demonstrated considerable changes. A considerable reversal of inflammation and deterioration was seen in the KA-treated groups according to X-ray examination. The FTIR spectroscopy indicated the changes in the molecular makeup of tissues, modifications of biomolecules including proteins, lipids, and carbohydrates. Histopathological changes showed improvements in cellular infiltration in the paw, and inflammatory cell infiltration as well as chondrocyte irregularity on joint surface in the treatment groups While trichrome revealed suppressed collagen deposition and suppression of inflammation and tissue repair in paw and joint. In paw and joint tissues, the KA therapy up-regulated IκB-α expression while down-regulating TLR4, NF-κB, iNOS, and COX-2 expression. On the other hand, KA therapy greatly increased antioxidants and decreased oxidative stress indicators. According to Evans blue dye, the study shows that in the treatment groups' vascular permeability was intensely reduced in comparison to the diseased groups. Kaurenoic Acid appeared to have a high tendency for binding to protein targets, according to molecular docking research. KA was associated with drop in the cytokines such as TNF-α and IL-1β. In conclusion, KA significantly reduced inflammation in response to a gout attack induced by MSU