Molecular Docking Studies on Some 4,5-Dihydro-1h-Pyrazole Derivatives as Cyclooxygenase Inhibitors

Abstract

Objective: To examine the interactions of some 4,5-dihydro-1H-pyrazole derivatives, which are thought to have antiinflammatory effects, with cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes, docking studies were carried out on these enzymes.Material and Method: COX-1 enzyme (3KK6) and COX-2 enzyme (3LN1) were selected from the protein data bank for docking studies. The ligand and protein constructs were prepared using Autodock 1.5.6. AutoDock Vina was used to determining the binding affinity, and Discovery Studio 3.5 was utilised to analyse and display the docking results.Result and Discussion: As a result of the docking process on COX-1 and COX-2 enzymes, 4,5-Dihydro-1H-pyrazole derivatives were observed to interact with both enzymes. The 4,5-dihydro-1H-pyrazole ring was found to be important in its interactions with the COX-2 enzyme. The inclusion of a bulky group in the construct did not cause any problems in interaction with the COX-1 enzyme but eliminated some interactions with the COX-2 enzyme. To better elucidate the inhibition properties of enzymes, this study should be supported by in vitro and in vivo COX inhibition tests.

Mechanistic Evaluation of Antiarthritic Effects of Eupatilin in CFA-Induced Arthritic Rats: An in Vivo and in Silico Study

“…The interactions shown by Eupatilin was discovered to be analogous to the interaction induced by celecoxib in the active site of COX-2. 42 Thus, it was suggested that, Eupatilin was proposed to interact with COX-2 in a manner similar to celecoxib by binding to the same active site.…”

“…The interactions shown by Eupatilin was discovered to be analogous to the interaction induced by celecoxib in the active site of COX-2. 42 Thus, it was suggested that, Eupatilin was proposed to interact with COX-2 in a manner similar to celecoxib by binding to the same active site. Moreover, it would be prudent to assess the efficacy of Eupatilin on a genetically induced arthritis model in addition to the CFA-induced arthritis model, since the former somewhat resembles RA and serves as the study's primary limitation.…”