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. 2020 Jun 11;22(2):1527–1535. doi: 10.3892/mmr.2020.11224

Figure 1.

Figure 1.

TBMS1 suppresses the growth of glioma cells by inhibiting the PI3K/Akt signaling pathway. U251 and HA cells were incubated with 0–50 µg/ml of TBMS1 for 24, 48 or 72 h. (A) Cell viability was determined by MTT. **P<0.01 and ***P<0.001 vs. TBMS1 (at 24h, 0 µg/ml); ##P<0.01 and ###P<0.001 vs. TBMS1 (at 48 h, 0 µg/ml); &&P<0.01 and &&&P<0.001 vs. TBMS1 (at 72h, 0 µg/ml). (B) The expression levels and quantitative values of p-Akt (S473), p-Akt (T308) and total Akt in U251 cells were monitored by western blot analysis. U251 cells were treated with TBMS1 (30 µg/ml) in the presence or absence of PI3K/Akt inhibitor LY294002 for 24 h. *P<0.05, **P<0.01 and ***P<0.001 vs. TBMS1 (0 µg/ml). (C) The expression levels and quantitative values of p-Akt (S473), p-Akt (T308) and total Akt in U251 cells were monitored by western blot analysis. *P<0.05, **P<0.01 and ***P<0.001 vs. Control+DMSO; #P<0.05 vs. LY294002+DMSO; &P<0.05 vs. Control+TBMS1. (D) Cell viability was determined by MTT. ***P<0.001 vs. Control; #P<0.05 vs. LY294002; &P<0.05 vs. TBMS1. TBMS1, tubeimoside-1; p-, phosphorylated.