Abstract
Baicalein (BAI) is a natural flavonoid. It has been shown that BAI has anticancer effects, but the molecular mechanism is still unclear. The aim of the current study was to confirm whether or not BAI triggers autophagy and induces AMPK activation in glioma U251 cells. The Ad-mcherry-GFP-LC3B adenovirus experiments indicated that BAI induces glioma cell autophagy. Western blotting showed that the level of LC3II expression increased with the time and concentration of BAI. Following treatment with chloroquine, the expression of LC3 was enhanced Immunofluorescence also confirmed this result. At the same time, cleaved caspase-3, DAPI staining, and JC-1 staining revealed that apoptosis was also induced in the induction of autophagy. In addition, we found that BAI activates phosphorylation of AMPK, which is further confirmed using compound C in this process. When the phosphorylation of AMPK was inhibited, autophagy, and apoptosis were also inhibited. In conclusion, BAI induces autophagy and apoptosis through AMPK pathway. Surprisingly, our research provides new insight with the function of anticancer of BAI, and the potential of the promotion in glioma cell apoptosis might be related to autophagy activation. These results demonstrate the anticancer activity of BAI, which can be used as potential therapeutic agents for cancer therapy.