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. 2015 Mar 27;22(11):1742–1753. doi: 10.1038/cdd.2015.20

Figure 2.

Figure 2

RSV prevents ROS production and mitochondrial dysfunction through SIRT1-dependent and -independent mechanisms in X-ALD fibroblast. (a) ROS production measured in control (CTL) and X-ALD fibroblasts treated with 50 μM of C26:0, 25 μM of RSV and 10 μM of EX-527 for 24 h. ROS values were normalized to untreated cells (n=6 per genotype and condition). (b) Galactose-induced cell death in CTL and X-ALD fibroblasts treated with 25 μM of RSV and 10 μM of EX-527 for 150 h (n=6 per genotype and condition). (c) ATP content in CTL and X-ALD fibroblasts treated with 25 μM of RSV and 10 μM of EX-527 for 136 h (n=6 per genotype and condition). (d) Percentage of cells with inner mitochondrial membrane depolarization in CTL and X-ALD fibroblasts treated with 25 μM of RSV and 10 μM of EX-527 for 136 h (n=6 per genotype and condition). (e) ROS production in CTL and X-ALD fibroblasts treated with 25 μM of RSV and 10 μM of EX-527 for 136 h (n=6 per genotype and condition). ROS values were normalized to untreated cells. Values are expressed as mean±S.D. (*P<0.05, **P<0.01 and ***P<0.001, one-way ANOVA followed by Tukey's HSD post hoc)