Potential Antibacterial of Leaf Sirih Merah Against Enterococcus Faecalis ATCC 29212 Bacteria.

Abstract

Background: Dental root canal failure is a disease caused by gram-positive bacteria, Enterococcus faecalis. The disease is caused by the bacterial cell wall consisting of a peptidoglycan layer that protects the bacteria from internal osmotic pressure. Peptidoglycan biosynthesis includes many enzymes, such as MurA, Penicillin-binding protein (PBP), and SrtA. Herbal plants are a source of bioactive compounds, including antibacterial agents. There is information that red betel leaves, also known as Piper crocatum, contain active substances such as flavonoids, terpenoids, and steroids. However, there is no additional information on the antibacterial properties of P. crocatum and the molecular mechanisms that affect the cell wall of E. faecalis ATCC 29212 bacteria.

Objective: This study aims to determine the antibacterial activity of the extract in vitro, screen and study the antibacterial compounds of red betel leaves against oral pathogenic bacteria, namely E.faecalis ATCC 29212 through molecular docking.

Methods: The n-hexan:ea (9:1) fraction of P. crocatum extract was tested for inhibition zones against E. faecalis ATCC 29212 bacteria, fractions that had positive results were then identified using the LC-MS method. The LC-MS resulting compounds were tested using In Silico.

Results: Antibacterial in the n-hexane: ethyl acetate (9:1) fraction of Red Betel Leaf has the best concentration of 10% with a moderate inhibition zone category. LC-MS test results identified compounds including Longicamphenylone, m/z 207, Nootkatone m/z 219, and Tridecanal m/z 221. Molecular interactions between these compounds with target proteins, namely MurA, PBP, and SrtA, show lower binding affinity values than natural ligands and positive controls for each protein.

Conclusion: Nootkatone compounds demonstrated potential as MurA and PBP inhibitors, while Longicamphenylone compounds showed potential as SrtA inhibitors. Both compounds have the potential to inhibit peptidoglycan biosynthesis and bacterial cell wall formation through docking simulations.