Fig. 10: Nicotine inhibited oxidative stress and protected Telomere stability of ageing mice.

a Nicotine 1, 10, 100 ng/mL regulated trolox-equivalent antioxidant capacity (TEAC) in HT22 cells treatment for 48 h (n = 3 biologically independent samples/group). b Nicotine 1, 10, 100 ng/mL regulated CuZn-Mn superoxide dismutase (CuZn-Mn SOD) activity in HT22 cells for 48 h (n = 3 biologically independent samples/group). c Nicotine decreased the carbonyl content in brain (n = 3, biologically independent samples/group), heart, liver (n = 3, biologically independent samples/group), and muscle of aged mice administered nicotine from 7 to 13 months. d Telomere length/single copy gene (T/S) ratio of β-galactose-induced (n = 3 biologically independent samples/group) aged HT22 cells after nicotine treatment (n = 3, biologically independent samples/group) for 7 days. e Nicotine increased the T/S ratio of heart, liver, muscle and bone marrow in aged mice administered nicotine for 6 months (n = 3, biologically independent samples/group). f Western blot and g were quantification of the telomere shelterin complex of brain, liver, kidney, muscle and spleen after 6 months nicotine administration. Quantification is normalized to GAPDH. Data are means ± SEM. p values were determined by one-way ANOVA with Tukey’s multiple comparisons tests (a, b, d) or two-way ANOVA analysis and Fisher’s least significant difference (c, e, g).