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. 2017 Aug 31;7:10270. doi: 10.1038/s41598-017-10619-0

Figure 3.

Figure 3

Expression and distribution of Atg16L1 after SE. (A) Western blotting analysis of Atg16L1 expression in the hippocampus of SE rats. Equal levels of protein samples (20 μg) were loaded, and β-actin served as a loading control. The relative optical density (Atg16L1/β-actin) were analyzed and represented as the mean ± SD (n = 3; **p < 0.01, compared with the ctrl group). (B) The cell type specificity of Atg16L1 was performed with double fluorescent immunolabeling (TRITC-labeled, red), accompanied with the astrocyte-specific marker GFAP (FITC-labeled, green). The nucleus was stained by DAPI (blue). Scale bar = 50 μm. The percent of GFAP and Atg16L1 positive cells was analyzed (n = 5; ns, no significant difference compared with the ctrl group). (C) The cell type specificity of Atg16L1 was performed with double fluorescent immunolabeling (TRITC-labeled, red), accompanied with the GFAP (FITC-labeled, green). The nucleus was stained by DAPI (blue). Scale bar = 50 μm. The percent of GFAP and Atg16L1 positive cells was analyzed (n = 5; **p < 0.01, compared with the ctrl group). (D) The cell type specificity of Atg16L1 was performed with double fluorescent immunolabeling (TRITC-labeled, red), accompanied with the neuron-specific marker NeuN (FITC-labeled, green). The nucleus was stained by DAPI (blue). Scale bar = 50 μm. The percent of NeuN and Atg16L1 positive cells was analyzed (n = 5; **p < 0.01, compared with the ctrl group).