Targeting VEGFR2 And COX-2: In Silico Assessment Of Quercetin And Gallic Acid From Saraca Asoca For Enhanced Wound Healing And Anti-Inflammatory Response

Abstract

This research was designed to explore the possible activities of quercetin and gallic acid, two pharmacologically active focus constituents on Saraca Asoca interaction with the wound and healing inflammation: angiogenesis process through endothelial molecular growth docking factor simulations of vascular receptor 2 (VEGFR2) and cyclooxygenase-2 (COX-2).

It has a strong binding affinity for VEGFR2 with a docking energy of -9.3  kcal/mol and forms hydrogen bonds with key residues like Cys919 and Glu917 with other polar interactions. Notable VEGFR2 binding is also exhibited by gallic acid with docking energy at -6.0 kcal/mol, forming three hydrogen bonds to all the significant residues. For the enzyme COX-2, the active site of quercetin was totally occupied with a docking energy of -7.4 kcal/mol through a number of hydrogen bonds that the molecule interacts with residues Lys83 and Tyr115 and more. Similar to the above case, gallic acid showed considerable binding with a docking energy of -6.5 kcal/mol and interacted with residues Thr206, His207, and Tyr385.

These results indicate that quercetin and gallic acid can interact with VEGFR2 and COX-2 effectively, modulating pathways that are critical for wound healing. Higher binding affinities of quercetin have made it a promising lead compound for further studies.

This study presents good evidence of the potential of Saraca Asoca isolates as therapeutics in wound care. Experimental studies should further confirm these results and further describe the mechanisms behind their pharmacological effects.