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Fig. 1 | Molecular Brain

Fig. 1

From: Genetic deletion of nitric oxide synthase 2 ameliorates Parkinson’s disease pathology and neuroinflammation in a transgenic mouse model of synucleinopathy

Fig. 1

Deletion of nos2 alleviates synuclein pathology and neuroinflammatory responses in SynA53T/NOS2−/− mice. A Immunofluorescence staining of the substantia nigra (SN), deep mesencephalic nucleus (DpMe), and granular insular cortex (Gi) of 10- to 11-month-old nTg, SynA53T, and SynA53T/NOS2−/− mice with an anti-p-Synser129 antibody. B Quantification of the data in A (SN, DpMe, Gi region; nTg: n = 17–20 brain slices/5 mice; SynA53T: n = 20–22 brain slices/5 mice; SynA53T/NOS2−/−: n = 14–16 brain slices/4 mice). C Immunofluorescence staining of the SN, DpMe, and Gi of 10- to 11-month-old nTg, SynA53T, and SynA53T/NOS2−/− mice with an anti-Iba-1 antibody. D Quantification of the data in C (SN, DpMe, Gi region; nTg: n = 20 brain slices/5 mice; SynA53T: n = 17–20 brain slices/5 mice; SynA53T/NOS2−/−: n = 11–15 brain slices/4 mice). E Immunofluorescence staining of the SN, DpMe, and Gi of 10- to 11-month-old nTg, SynA53T, and SynA53T/NOS2−/− mice with an anti-GFAP antibody. F Quantification of the data in E (SN, DpMe, Gi region; nTg: n = 20 brain slices/5 mice; SynA53T: n = 17–20 brain slices/5 mice; SynA53T/NOS2−/−: n = 12–16 brain slices/4 mice). G Differentially expressed genes (DEGs) were identified by comparing SynA53T/NOS2−/− mice with SynA53T mice and SynA53T mice with nTg mice. The numbers of DEGs in each comparison and the number of overlapping DEGs are indicated. H Six clusters (C1–6) of DEGs were identified from the two comparisons. The color bar represents the gradient of log2 fold changes. The number of DEGs in each cluster is denoted in parentheses. I Cellular processes represented by the DEGs in C2. The x-axis is the −log10(P), where P is the enrichment P value from ConsensusPathDB software. J DEGs involved in the inflammatory response (n = 3 mice/group). *p < 0.05, **p < 0.01, ***p < 0.001, scale bar = 100 μm

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