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. 2016 Mar 3;291(18):9733–9747. doi: 10.1074/jbc.M115.687806

FIGURE 6.

FIGURE 6.

Activation of ERK, AKT, STAT3, and NFκB-p65 are involved in NO-mediated hCSC survival with essential functional roles. hCSCs were treated with various pharmaceutical inhibitors to specifically block cell survival signaling activity. Cells treated with vehicle or DETA-NO preconditioning were challenged with H2O2 and then examined by LDH release assay. A, Bay117085 (5 μm) was applied to inhibit NFκB activity. B, STATTIC (1 μm) was applied to inhibit STAT3 activity. C, U0126 (10 μm) was applied to inhibit ERK activity. D, LY294002 (10 μm) was applied to inhibit PI3K activity. E, AKT IV (0.2 μm) was applied to inhibit AKT activity. Data are presented as means ± S.D. from four independent experiments. Error bars represent S.D. *, p < 0.05; **, p < 0.01; and ***, p < 0.001 versus the indicated control group.