Apoptosis induced by baicalin involving up-regulation of P53 and bax in MCF-7 cells.

Anticancer effect of baicalin (1) has been well documented. However, the molecular mechanisms underlying the cytotoxicity of baicalin in cancer cells remain unclear. In the present study, we examined the potential roles of p53, bax, and bcl-2 in baicalin-triggered apoptosis in MCF-7 cells, a cell line derived from human breast cancer. The results showed that cell proliferation was significantly inhibited by baicalin in a dose- and time-dependent manner. Flow cytometric analysis also revealed that most of the baicalin-treated MCF-7 cells were arrested in the G(0)/G(1) phase. Significant amount of cells underwent apoptotic cell death 24 h following baicalin treatment. Typical apoptotic characteristics such as chromatin condensation and the formation of apoptotic bodies were noted 48 h following baicalin exposure. Semi-quantitative analysis using RT-PCR revealed dramatic elevation of mRNA levels of proapoptotic molecules p53 and bax, but not the anti-apoptotic bcl-2. Consistently, significant elevation of p53 and bax was substantiated by the western blot. Collectively, the data demonstrated that baicalin-induced apoptotic cell death in the breast cancer cells involves the up-regulation of proapoptotic p53 and bax, implying potential crucial roles of bax and p53 in the baicalin-induced apoptosis.