MAIN METHODS: Colon cancer HCT-116 cells were treated with 8-PN and subjected to MTT and acridine orange/propidium iodide (AO/PI) staining to investigate the cytotoxicity of 8-PN. Arrest of the cells at different phases of cell cycle was monitored in the presence of 8-PN. Moreover, the apoptotic effects of 8-PN was assessed via annexin V and caspase activity assays and compared to the untreated cells.
KEY FINDINGS: The findings showed that 8-PN revealed strong inhibitory effect against HCT-116 cells with an IC50 value of 23.83 ± 2.9 μg/ml after 48 h. However, at similar concentrations and experimental time-points, the compound did not show cytotoxic effect to non-cancerous colon cells (CCD-41). Annexin-V assay indicates that 38.5% and 14.4% of HCT-116 cells had entered early and late stages of apoptosis, respectively after exposure of the cells to 8-PN for 48 h. Caspase activity assay illustrates that apoptosis is activated through both intrinsic and extrinsic pathways. Moreover, flow cytometry cell cycle results indicate that treatment with 8-PN significantly arrested the HCT-116 cells at G0/G1 phase.
SIGNIFICANCE: These findings reveal that 8-PN has anti-proliferative activity against HCT-116 colon cancer cells via induction of intrinsic and extrinsic pathway-mediated apoptosis. Further investigations should be carried out to unravel the mechanistic pathways underlying these activities.
Methods: Anti-cholinesterase, anti-oxidant, and total phenolic and flavonoid contents were established using standard procedures.
Results: The three polyherbal extracts exhibited significant concentration dependent acetylcholinesterase (AChE) inhibitory activity (P = 0.001). The highest AChE inhibition was observed with the Neocare Herbal Tea (NHT) with 99.7% (IC50 = 324 μg/mL); whereas the Herbalin Complex Tea (HCT) and Phytoblis Herbal Tea (PHT) exhibited 73.8% (IC50 = 0.2 μg/mL) and 60.6% (IC50 = 0.7 μg/mL) inhibition, respectively, relative to eserine at 100% inhibition (IC50 = 0.9 μg/mL) at 200 μg/mL. The order of percentage increase in inhibition of AChE was NHT > HCT > PHT; while the order of decrease in potency was HCT > PHT > NHT.Radical scavenging activities of HCT, NHT and PHT were 82.13% (IC50 = 0.08 μg/mL), 77.43% (IC50 = 0.01 μg/mL) and 76.28% (IC50 = 0.3 μg/mL), respectively, at 1 mg/mL concentrations. The reducing power revealed a dose-dependent effect, with NHT > PHT > HCT. The order of total phenolics content in the extracts were PHT > HCT > NHT, and for total flavonoids content: PHT > NHT > HCT.
Conclusion: The three polyherbal standardised products possess significant acetylcholinesterase inhibitory activity and secondary metabolites that could collectively contribute to their memory-enhancing effects.
Methods: Proliferation and apoptosis studies of U-87 MG cells following stingless bee honey treatment were carried out using MTS assay and acridine orange/propidium iodide dual staining, respectively.
Results: Results demonstrated time and dose-dependent cytotoxicity using 0.625%, 1.25% and 10% stingless bee honey (P < 0.05). IC50 values were calculated using cells treated with 10% stingless bee honey. It was also observed that 10% stingless bee honey induced nuclear shrinkage, chromatin condensation and nucleus fragmentation, indicating that cellular changes were consistent with the apoptotic characteristics of the cells.
Conclusion: These data provide a good basis for further evaluation of the medicinal properties of stingless bee honey from Heterotrigona itama sp. This source of honey may serve as a potential therapy for malignant glioma.