reatment promoted myenteric neuronal survival and ameliorated nerve fiber and glial cell density in the myenteric plexus in Winnie mice. A, Neuronal microtubule proteins were labeled by immunofluorescence using β-tubulin (III; purple) antibody to identify nerve fibers innervating the colon in cross-sections (scale bar = 100 µm, 20x magnification). Anti-MAP2-IR antibody staining (blue) for myenteric neurons in LMMP preparations (scale bar = 50 µm, x40 magnification). Glial cells were labeled with an anti-GFAP antibody (orange) in the myenteric plexus of the colon from C57BL/6 control, Winnie sham-treated, and Winnie APX3330-treated mice (scale bar = 50 µm, 40x magnification). B, Density of β-tubulin (III)-IR nerve fibers normalized to colon thickness in C57BL/6 control, Winnie sham-treated, and Winnie APX3330-treated mice (n = 5/group). C, Quantitative analysis of myenteric neurons per ganglion C57BL/6 control, Winnie sham-treated, and Winnie APX3330-treated mice (n = 5/group). D, Myenteric neurons were quantified per area in LMMP preparations of C57BL/6 control, Winnie sham-treated, and Winnie APX3330-treated mice (n = 5/group). E, Density of GFAP-IR glial cells per ganglia in C57BL/6 control, Winnie sham-treated, and Winnie APX3330-treated mice (n = 5/group). Data expressed as mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, compared with C57BL/6 control mice; ^P < 0.05, ^^P < 0.01, ^^^P < 0.001 compared with Winnie sham-treated mice.