KEY FINDINGS: The phytochemical investigations of Ferulago species revealed the presence of coumarins as the main bioactive compounds, including daucane derivatives, sesquiterpenes aryl esters, phenol derivatives, flavonoids and essential oils. Moreover, the therapeutic potentials of the pure compounds isolated from the genus Ferulago possess promising properties namely anticholinesterase, antimicrobial, anticoagulant, antileishmanial, antioxidant, antibacterial and antiproliferative.
SUMMARY: Today, significant advances in phytochemical and biological activity studies of different Ferulago species have been revealed. The traditional uses and reported biological results could be correlated via the chemical characterization of these plants. All these data will support the biologists in the elucidation of the biological mechanisms of these plants.
METHODS: The cytotoxic activity of AKBA was measured by 3(4,5dimethylthiazole- 2-yl)-2,5 diphyneltetrazolium bromide (MTT) assay. A dose-dependent inhibition in MCF-7 cell viability was detected. The clonogenicity of MCF-7 cells was significantly suppressed by AKBA increment in comparison with untreated cells.
RESULT: Morphologically, exposure of MCF-7 cells to high AKBA concentrations caused changes in cell nuclear morphology which was indicated by increasing in nuclear size and cell permeability intensity. The mitochondrial membrane potential (ΔΨm) was reduced by increasing AKBA concentration with a significant release of cytochrome c. Acridine orange/ethidium bromide dual staining experiment confirmed that MCF-7 cells treated with AKBA (IC50 concentration) displayed a late stage of apoptosis indicated by intense and bright reddish colour.
CONCLUSION: A significant increase in reactive oxygen species formation was observed. Caspase 8 and caspase 9 activities were estimated and AKBA activated the production of caspase 8 and caspase 9 in a dose-dependent pattern. Finally, the cell phase distribution analysis was conducted, and flow cytometric analysis showed that AKBA at 200 μg mL-1 significantly arrest MCF-7 cells at the G1 phase and triggered apoptosis.