In vitro and in vivo evaluation of the antiangiogenic activities of Trigonella foenum-graecum extracts

Objective To assess the antiangiogenic activity of fenugreek. Methods Different fractions of fenugreek crude extracts were prepared and their antiangiogenic properties were assessed using the ex vivo rat aortic ring assay and in vivo chicken embryo chorioallantoic membrane (CAM) assay. They were investigated for their direct cytotoxic activity in the MCF7 cells using the MTT assay. Results The ethanol extract showed 100% inhibition of blood vessel outgrowth from primary tissue explants in the rat aortic ring assay at a concentration of 100 μg/mL while the other extracts did not show significant antiangiogenic activity. The ethanol extract was therefore investigated at varying concentrations and exhibited a significant dose dependent effect. The CAM assay coincided with the results of the aortic ring assay as ethanol extract showed a significant inhibition of formation of new blood vessels. The extracts only showed anti-proliferative activity at the highest concentration of 400 μg/mL towards MCF7 breast cancer cell lines in the MTT assay. Conclusions Findings of the both assays confirmed that the ethanol extract inhibited vascularization significantly. Further studies on the ethanol extract would be beneficial in isolating the active ingredient responsible for the inhibition.

Some insights into the cellular responses against doxorubicin and actinomycin D

Cellular responses to anti-cancer agents are an important factor in recognizing mechanisms of resistance and in identifying new treatment biomarkers. In this study, we have compared the effect of actinomycin D and doxorubicin on selected genes in the transcription and ubiquitin pathways. The human promyelocytic leukemia cells [HL60] was used as a model system and the chosen genes were POL2A and ELL2 [from transcription machinery] and UBE2DE and CDC [from ubiquitin pathway]. The responses of the four targeted genes suggested a degree of biological resistance amongst just those functions that might be expected to be damaged by the drug action. It is as if the cells are trying to upregulate these functions to offset drug inhibition. For example, doxorubicin up-regulated ubiquitinrelated genes suggesting an attempt to remove the trapped cleavable complex by an ubiquitin-dependent mechanism, while actinomycin up-regulated the transcription machinery genes suggesting an attempt to overcome the longed lived complexes that are formed by the actinomycin D on the DNA