Skip to main content
. 2021 May 19;46(1):138–146. doi: 10.1016/j.jgr.2021.05.005

Fig. 1.

Fig. 1

Rg3-RGE suppress proliferation of lung cancer cells. (A) A549 and H460 cells were treated with different concentrations of Rg3-RGE for 24h. Cell viability was measured by WST-8 and LDH assays. The experiment was repeated in triplicate. Results represent means ± SE. ∗,#: p < 0.05 or ∗∗,##: p < 0.01 ∗∗∗,###: p < 0.001 versus controls. (B) A549 and H460 cells were treated with the indicated concentrations of Rg3-RGE for 24h. Cell colonies were detected by crystal violet staining and counted. Data represent means ± SD of three independent experiments. ∗: p < 0.05 or ∗∗: p < 0.01 versus controls. (C) A549 and H460 cells were treated with the indicated concentrations of Rg3-RGE for 24 h. Protein expression levels of cleaved caspase3 and PARP were analyzed by western blotting. (D) Rates of apoptosis in A549 and H460 cells treated with Rg3-RGE (200 μg/ml) for 24 were detected by flow cytometry. (E) Caspase 3 activity was detected after treatment with Rg3-RGE (200 μg/ml) for 24 h. (F) A549 and H460 cells were treated with Rg3-RGE (200 μg/ml) for 24h, and cell lysates were divided into cytoplasmic and mitochondrial fraction. Protein expression levels of cytochrome c were analyzed by western blotting. β-actin and PCNA were used as loading controls.