Baicalein is an antioxidant and had been demonstrated to induce apoptosis in human cancer cell lines. However, the exact molecular mechanism of apoptosis induced by baicalein in human liver cancer J5 cells is unclear. In this study, we investigated the cell cycle arrest and apoptosis occurrence in J5 cells after exposed to baicalein by flow cytometry. We also used DAPI stain、comet assay、confocal and western blot to detect the mechanisms. The result from flow cytometric analysis demonstrated that caused G2/M-phase arrest by phosphorylation cdc25c and cdc2 inhibit activity of cdc2-cycin B1 complex. Flow cytometric analysis indicated that baicalein promoted the increase of reactive oxygen species (ROS) and Ca2+ in J5 cells. Baicalein also decreased the levels of mitochondrial membrane potential from J5 cells. We also detect cytochrome c、AIF and endo G release from mitochondria, indicated that baicalein elicited a significant increase of DNA fragmentation in J5 cells and promote the cell apoptosis. We also detect increase expression of caspase-9 and caspase-3. In this study, we also used NAC (ROS inhibitor) to decrease ROS and apoptosis generation. Baicalein cause oxidative stress production and Ca2+ release from ER and promote GADD153 and GRP78 expression.
Matrix metalloproteinase (MMPs), one of the families of enzymes that degrade the extracellular matrix (ECM), are considered to play an important role of tumor invasion and spread. We have demonstrated that baicalein inhibits the invasion of human liver cancers by suppressing MMP-9 expressions.
