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Fig. 6 | Molecular Brain

Fig. 6

From: Decreased expression of the clock gene Bmal1 is involved in the pathogenesis of temporal lobe epilepsy

Fig. 6

Bmal1 and PCDH19 expression in the hippocampal DG of patients with TLE. A, B Detection of the endogenous Bmal1 and PCDH19 protein (red) in DG of HS type I, HS type III, and no HS by immunofluorescent labeling. Neurons were labeled by the neuronal marker, NeuN (green). Scale bar, 100 μm. C Analysis of fluorescence intensity was performed using ImageJ. Differences in the relative fluorescence intensity (Bmal1 vs. NeuN) among the three groups were analyzed with one-way ANOVA, compared with no HS (HS I: 0.741 ± 0.060, HS III: 0.860 ± 0.651, no HS:1.059 ± 0.081, n = 5). D Differences in the relative fluorescence intensity (PCDH19 vs. NeuN) among the three groups were analyzed with one-way ANOVA, compared with no HS (HS I: 0.739 ± 0.079, HS III: 1.044 ± 0.093, no HS:1.160 ± 0.157, n = 5). E The levels of Bmal1 and PCDH19 protein in the hippocampus of HS type I, HS type III, and no HS by immunoblotting. F Differences in the levels of Bmal1 among the three groups were analyzed with one-way ANOVA, compared with no HS (For Bmal1, HS I: 0.350 ± 0.062, HS III: 0.494 ± 0.106, no HS:1.000 ± 0.135, n = 6; For PCDH19, HS I: 0.379 ± 0.037, HS III: 0.501 ± 0.102, no HS:1.000 ± 0.105, n = 6;). *p < 0.05, **p < 0.01

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