RESUMO
Aim To explore the inhibitory effect of ar-temisinin on hepatocellular carcinoma cells and its anti-hepatocarcinoma mechanism. Methods Different concentrations of artemisinin were cultured with human hepatoma cell line HepG2 for 24 h, 48 h and 72 h. Cell viability assay was used to detect cell proliferation activity. Cell clone assay was used to detect inhibition. Cell flow assay was used to detect apoptosis. Western blot and immunofluorescence assay were used to detect changes of intracellular beta p-catenin protein content in HepG2 cells. Results Artemisinin inhibited the proliferation of HepG2 cells in a time- A nd dose-de-pendent manner. Compared with blank control, artemisinin significantly inhibited the proliferation of HepG2 cells (P < 0. 05) , and artemisinin induced ap-optosis of HepG2 cells. It was found that artemisinin inhibited the transition of epithelial cells to mesenchymal cells by increasing the content of p-catenin in the cytoplasm of HepG2. Conclusions Artemisinin can inhibit the proliferation of HepG2 cells and the metastasis of hepatoma cells, which may be through the inhibition of the transport of p-catenin from the cytoplasm to the nucleus, thereby inhibiting EMT.