In Vitro Antioxidant and Anti-Colon Cancer Activities of Sesamum indicum L. Leaf Extract and Its Major Component, Pedaliin.

Sesame (Sesamum indicum L.) leaves (SLs) are used as vegetables and traditional medicines in Asian and African countries. We investigated in vitro antioxidant and anti-colon cancer efficacy of ethanol extract of SL (SLE) and its major bioactive component. SLE contained appreciable amount of major classes of antioxidant phytochemicals, such as total polyphenols, total flavonoids, and carotenoids, and correspondingly exhibited antioxidant activities, such as radical scavenging activity and ferric reducing antioxidant power (FRAP). A cell viability assay showed that SLE time- and dose-dependently attenuated the growth of human colon cancer cells, HT29 and HCT116. Flow cytometry analysis showed that SLE increased sub-G1 (in HT29 and HCT116) and G2/M (in HCT116) cell populations, suggesting that the growth inhibition by SLE was due to induction of apoptosis and G2/M cell cycle arrest. Trans-well and wound-healing assays showed that SLE alleviated invasion and migration of HT29 and HCT116 cells in non-cytotoxic conditions. High-performance liquid chromatography analysis revealed that pedaliin (6-hydroxylueolin 7-methyl ether 6-glucoside; pedalitin-6-O-glucoside) was a major constituent of SLE. Moreover, FRAP, growth-inhibitory, anti-invasive, and anti-migratory activities of pedaliin were found. These results demonstrated that SLE possesses in vitro antioxidant and anti-colon cancer activities and that pedaliin is a major component contributing to such activities.

Antirrhinum majus L. flower extract inhibits cell growth and metastatic properties in human colon and lung cancer cell lines.

Snapdragon ( Antirrhinum majus L.) flowers are one of the most frequently used edible flowers in different preparations of foods and drinks. In this study, we examined inhibitory effects of snapdragon flower extract (SFE) against distinctive properties of cancer cells, stimulated growth, and activated metastasis, using H1299 lung cancer and HCT116 colon cancer cell lines. SFE treatment at 100-1,000 µg/ml for 24-72 hr resulted in a time- and dose-dependent growth inhibition in H1299 and HCT116 cells. Cell cycle analysis and Annexin V staining assay further revealed that SFE caused cell cycle arrest at G2/M phase and induction of apoptosis, indicating the growth inhibition by SFE is attributed to its G2/M cell cycle-arresting and apoptosis-inducing activities. SFE dose-dependently enhanced generation of intracellular reactive oxygen species (ROS) and reduced mitochondrial membrane potential in H1299 cells but had no effect on intracellular ROS levels in HCT116 cells, suggesting that the type of apoptosis induced by SFE in H1299 cells is different to that in HCT116 cells. Furthermore, SFE alleviated invasion, levels of matrix metalloproteinases, migration, and adhesion in H1299 and HCT116 cells. These results indicate that SFE not only inhibits cell growth by cell cycle arrest at G2/M and apoptosis induction but also alleviates metastatic properties such as invasion, migration, and adhesion in lung and colon cancer cells.