DeEA (10 [micro]g/g) was orally administered to the treatment group and the control group received solvent only.
The analytical and the biological assays clearly implied that 5 (DeEA) is FEA major component with the most potent apoptotic and DNA damaging activities.
The apoptotic and the DNA damaging activities of DeEA
To further confirm the fact that DeEA is the lead active compound of FEA (triterpenoid-rich fraction) the cytotoxicity of DeEA and FEA against HL 60 cells was compared (Fig.
Treatment of HL 60 cells with increasing doses of DeEA (0, 2.5, 5 and 10 [micro]g/ml) resulted in G2/M distribution rates of 21.1%, 26.6%, 28.7% and 39.5%, respectively after 24 h (Fig.
To clarify the role of DeEA as DNA damaging agent, we treated HL 60 cells with various concentrations of DeEA for 18 h and analyzed the level of tail movement with the alkaline cornet assay.
To examine the extent of DNA damage which can lead to the activation of cell cycle checkpoints in HL 60 cells, the effect of DeEA on PARP, p-H2A.X and p-Chk2 was studied (Fig.
The inhibitory activity of DeEA on topoisomerase II
The structure of dehydroebriconic acid is similar to DeEA except the hydroxyl group at C-3 in DeEA is replaced by a carbonyl group in dehydroebriconic acid.
The inhibitory activity of dehythoebriconic acid on DNA topo II encouraged us to examine whether DeEA treatment can induce DNA damage in leukemia cells through inhibition of topo II or not.
The inhibitory effect of DeEA on tumor growth in xenograft animal model