Figure 1

IL-1α and IL-1β significantly increased neurite outgrowth in normal and diabetic neurons. In (a) images of cultures stained for neuron-specific β-tubulin III are shown for untreated control (Ctl), treated for 24 h with IL-1β (10 ng/ml) or treated with IL-1α (10 ng/ml). Size marker indicates 100 μm. In (b) is shown total neurite outgrowth of neurons in response to a range of IL-1α concentrations grown for 24 h under defined conditions without neurotrophic growth factors (GF). Values are means ± SEM (n = 3 replicates); *p < 0.05 vs control (oneway ANOVA with Dunnett’s test). In (c) is shown total neurite outgrowth of neurons in response to a range of IL-1β concentrations without neurotrophic growth factors. Values are means ± SEM (n = 3 replicates); *p < 0.05 vs control (oneway ANOVA with Dunnett’s test). In (d) is shown total neurite outgrowth of neurons in response to a range of IL-1β concentrations in the presence of low dose cocktail of neurotrophic growth factors. Values are means ± SEM (n = 3 replicates); *p < 0.05 vs control (oneway ANOVA with Dunnett’s test). In (e) is shown total neurite outgrowth for sensory neurons isolated from control or 3–5 month STZ-diabetic rats cultured for 1 day ± IL-1β (at 10 ng/ml). Cultures were performed with or without neurotrophic factors. Values are the means ± SEM (n = 3 replicates). For control or diabetic *p < 0.05 vs control (Ctl) and **p < 0.05 vs Ctl (two-way ANOVA with Bonferroni’s test).