Affiliations 

  • 1 School of Medicine, International Medical University, Kuala Lumpur. Malaysia
  • 2 School of Health Sciences, International Medical University, Kuala Lumpur. Malaysia
Curr Pharm Biotechnol, 2021 Aug 05.
PMID: 34365946 DOI: 10.2174/1389201022666210806092643

Abstract

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) has been constantly evolving and developing resistance against conventional antibiotics. One of the key features of MRSA that enables it to develop resistance to antibiotics and host immune system is its ability to form biofilm in indwelling medical devices. In previous studies, the antimicrobial activity and mechanisms of action of three known pentacyclic triterpenoids α-amyrin, betulinic acid and betulinaldehyde against planktonic cells of MRSA were determined and elucidated.

OBJECTIVE: This study was carried out to evaluate the ability of the three compounds to significantly reduce the biomass of pre-formed biofilms of MRSA and metabolic activity of the bacterial cells in the biofilm.

METHODS: The anti-biofilm activity of α-amyrin, betulinic acid and betulinaldehyde, individually and in combination with oxacillin or vancomycin, against reference strain of MRSA in pre-formed biofilm were evaluated using the crystal violet and resazurin assays.

RESULTS: α-amyrin and betulinic acid significantly reduced the biomass of pre-formed biofilms of MRSA as individual compounds and in combination with oxacillin or vancomycin. Although betulinaldehyde individually increased the biomass, selected combinations with oxacillin and vancomycin were able to reduce the biomass. All three compounds did not show cytotoxic properties on normal mammalian cells.

CONCLUSION: The three pentacyclic triterpenoids could significantly reduce pre-formed biofilm of MRSA with no cytotoxic effects on normal mammalian cells. These findings demonstrated that pentacyclic triterpenoids have the potential to be developed further as antibiofilm agents against MRSA cells in biofilms, to combat infections caused by multidrug-resistant and biofilm-forming S. aureus.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.