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. 2020 Apr 6;117(16):9082–9093. doi: 10.1073/pnas.2000208117

Fig. 4.

Fig. 4.

UA enhances remyelination in cuprizone-induced demyelination in a PPARγ-dependent manner. (A) Treatment paradigms. Male, 8- to 10-wk-old C57BL/6J mice were fed with cuprizone (CUP) for 6 wk to achieve complete demyelination, followed by feeding PBS or UA (25 mg/kg/d) for another 2 wk. (B) Representative electron microscopy images of the corpus callosum region isolated from cuprizone-fed mice treated with UA or PBS for 2 wk. (C) Quantification of the myelinated axons. (D) Quantification of the G-ratios (axon diameter/fiber diameter) of myelinated fibers. (E) Representative LFB and FluoroMyelin stains in the body of the corpus callosum of UA- or PBS-treated WT or PPARγ+/− mice at 2 wk after cuprizone withdrawal. (F) Quantitative analysis of myelinated and fluoromyelinated areas measured in the body of the corpus callosum using Image Pro software. (G) Immunohistochemistry on corpus callosum sections of UA- or PBS-treated WT or PPARγ+/− mice at 2 wk after cuprizone withdrawal. (H) Quantitative analysis of GFAP, IBA1, A2B5, and CC1 expression using Image-Pro. Groups designated by the same letter are not significantly different, while those with different letters (a, b, c, or d) are significantly different (P < 0.05 to 0.01), one-way ANOVA with Tukey’s multiple comparisons test. All quantifications were made from three independent experiments. Symbols represent mean ± SD; n = 5 to 8 mice each group. (Scale bar, 2 µm in B, 100 µm in E, and 20 µm in G.)