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. 2022 Nov 10;23(22):13840. doi: 10.3390/ijms232213840

Figure 3.

Figure 3

Carvacrol suppressed dendritic injury after TBI: (A) Representative immunofluorescence images showing sections of hippocampus stained with MAP-2 antibody to detect neuronal dendrites. Nuclei are stained with DAPI (blue). Scale bar, 20 µm; (B–D) quantification of the immunofluorescence intensity of MAP-2 (green) as determined in the same CA1 (B), GCL (C), and hilus (D) regions of the ipsilateral hippocampus with or without carvacrol treatment in sham-operated and TBI groups (mean ± SEM; n = 3–6 per group). * p < 0.05 vs. vehicle-treated TBI group (Kruskal–Wallis test followed by Bonferroni post-hoc test: CA1: Chi square = 13.437, df = 3, p = 0.004; GCL: Chi square = 8.354, df = 3, p = 0.039; hilus: Chi square = 10.315, df = 3, p = 0.016); and (E–G) bar graphs showing the percentage areas of MAP-2 immunoreactivity, as determined in the same CA1 (E), GCL (F), and hilus (G) regions of the ipsilateral hippocampus with or without carvacrol treatment in sham-operated and TBI groups (mean ± SEM; n = 3–6 per group). * p < 0.05 vs. vehicle-treated TBI group (Kruskal–Wallis test followed by Bonferroni post-hoc test: CA1: Chi square = 14.242, df = 3, p = 0.003; GCL: Chi square = 14.765, df = 3, p = 0.002; hilus: Chi square = 14.294, df = 3, p = 0.003).