Abstract

The in vitro anti-gout arthritic activity of ethanolic and aqueous extracts of Cissus quadrangularis stem was evaluated in terms of inhibition of xanthine oxidase, proteinase enzyme, protein denaturation and membrane stabilization. The Monosodium Urate (MSU) up-regulated expression patterns of toll like receptors namely TLR-2and TLR-4 were analyzed. The molecular docking was performed to select the antagonistic phyto ligand for receptors since their activation leads to the destructive immunological reactions occurring in gouty arthritis. The in vitro anti-gout arthritic activities were estimated using standard protocols. The MSU crystal induced toll like receptors gene expression was analyzed. Molecular docking and LIGPLOT analysis was performed with the GCMS derived phyto constituents in the ethanolic extract of Cissus quadrangularis with the receptors to find the interactions. Colchicine was used as a positive drug in the study. Among the two extracts, ethanolic extract revealed better in-vitro anti arthritic activity in the present investigation. Out of the GCMS derived 13 phyto components, based on docking score three main components namely Pentadecanoic acid, 14-methyl,-methyl ester,10-Octadecenoic acid, methyl ester, 4-one,2-(3,4-dihydroxyphenyl)-2,3-dihydro-3,5,7-trihydroxy showed better antagonistic action in the LIGPLOT analysis. It may be concluded these three ligands may further developed as a potential anti gouty arthritic drug

Highlights

  • Gout is a metabolic disorder with a worldwide distribution that is associated with an excess of circulating levels of uric acid

  • The in vitro anti-gouty arthritic activity of ethanolic and aqueous extracts of Cissus quadrangularis stem was evaluated in terms of inhibition of xanthine oxidase, proteinase enzyme, protein denaturation and membrane stabilization

  • Molecular docking and LIGPLOT analysis were performed with the GCMS-derived phytoconstituents in the ethanolic extract of Cissus quadrangularis with the receptors to find the interactions

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Summary

Introduction

Gout is a metabolic disorder with a worldwide distribution that is associated with an excess of circulating levels of uric acid (hyperuricemia). This results in the formation and deposition of monosodium urate crystals (MSU) in the joints causing inflammatory arthritis and severe pain. Hyperuricemia can be caused by impaired renal excretion or overproduction of uric acid due to overconsumption of purine-rich foods. Xanthine oxidase enzyme is responsible for the hyperuricemia and goutby catalyzing the oxidation of xanthine and hypoxanthine into uric acid (Unno et al, 2004). The risk for supersaturation occurs and the urate crystallizes when the plasma concentration of monosodium urate (MSU) exceeds its solubility (around 7 mg/dl) concentration due to impaired glomerular filtration.

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