Oral Presentation Joint Annual Scientific Meeting of the Nutrition Society of NZ and the Nutrition Society of Australia

Bioactive fractioning of Ganoderma lucidum triterpenoids show cell specific effects on cancer cell growth (303)

Weimei Ruan 1 , David Popovich 2
  1. Institute of Molecular and Cell Biology , Agency for Science, Technology and Research, Singapore
  2. School of Food and Nutrition, Massey University, Palmerston North, New Zealand

Background/Aims: Ganoderma lucidum is an edible mushroom with a long history of use in traditional Chinese medicine.  The mushroom has been associated with a variety of pharmaceutical activities and it is thought that the triterpenoids are the main active group with chemo preventative properties.  

Methods: We have utilized a bioactive fraction protocol to identify six triterpenoids by ESI-MS and NMR and were tested in three distinct cultured human cancer cell lines. The aim was to assess the effect of purified triterpenoids on cultured cancer cell growth

Results: Six compounds (ganodermanontriol, ganolucidic acid E, lucidumolA, 7-oxo-ganoderic acid Z, 15-hydroxy-ganoderic acid S, ganoderic acid DM) reduced cultured cancer cell growth in three cancer cell lines colon (Caco-2), the liver (Hep-G2) and the cervix (HeLa) to varying degrees. LC50 ranged from 20.87 µM – 84.36 µM.  Ganodermanontriol had the greatest inhibitory effect in HepG2 cells with an LC50 of 20.87±1.48 µM, while 15-hydroxyl-ganoderic acid S exhibits the most cytotoxicity in HeLa and Caco-2 cells with LC50s of 21.17 ± 1.81 and 30.38 ± 1.44 µM respectively.  Apoptotic cell death was observed for all compounds tested in Hela cells with 15-hydroxy-ganoderic acid S showing the greatest sub-G1 cells (22%) in cell cycle analysis and apoptotic positive cells in TUNEL assay (43.03%). These results were confirmed by annexin-V staining.  Interestingly, none of the compounds induced apoptosis in Hep-G2 cells.

Conclusion: Bioactive triterpenoids from Ganoderma lucidum induce apoptosis and likely trigger different cell death pathways which are dependent on tissue type and function.

Funding source(s): N/A