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. 2015 May 29;36(2):415–423. doi: 10.3892/ijmm.2015.2229

Figure 3.

Figure 3

Nicorandil activates the PI3K/Akt signaling pathway under H/SD conditions. MSCs were treated with nicorandil (100 μM) for the indicated periods of under H/SD conditions for 9 h. (A and C) The levels of p-Akt was upregulated by nicorandil in a time-dependent manner, peaking at 90 min. Data are presented as the means ± SD of 3 separate experiments. *P<0.05, compared with the normal group; ▲P<0.05, compared with the group treated with nicorandil for 90 min. (B and D) The inhibition of PI3K with LY294002 triggered p-Akt inactivation. (E and F) Nicorandil induced a significant decrease in the apoptotic rate of MSCs under H/SD conditions, which was reversed by LY294002. Data are presented as the means ± SD of 3 separate experiments. *P<0.05, compared with the normal group; ▲P<0.05, compared with the 100 μM nicorandil-treated group. PI3K, phosphoinositide 3-kinase; MSCs, mesenchymal stem cells; H/SD, hypoxia/serum deprivation; Nico, nicorandil; p-Akt, phosphorylated Akt (Ser473); t-Akt, total Akt; NAC, N-acetyl-L-cysteine.