The Anti-Inflammatory Agent Bindarit Attenuates the Impairment of Neural Development through Suppression of Microglial Activation in a Neonatal Hydrocephalus Mouse Model

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Figure 1.
Figure 1.

Inflammation and myeloid cell involvement in prh hydrocephalic mouse brains. A, The Mcp-1 (**p = 0.0057), tumor necrosis factor (Tnf)-α (*p = 0.019), Tlr-4 (*p = 0.0310), Hmox-1 (*p = 0.0464) mRNA expression relative to housekeeping gene Gapdh mRNA are significantly upregulated in prh relative to that in WT mouse brains (without treatment, P8–P10, Student's t test, n = 5–6 in each group). B, Mcp-1 mRNA in nontreated prh is well correlated with the severity of ventricular size (R2 = 0.7385, n = 12). C, Volcano plot of differentially expressed genes (DEGs) in P8 prh brains relative to WT (data based on n = 6 in each group). Adjusted p value < 0.5 is shown. D, DEGs with nominal p value < 0.01. E, nSolver pathway analysis based on REACTOME pathway identified 16 gene sets upregulated in prh (blue), and gene enrichment analysis with cell type signature gene sets (C8) identified five gene sets enriched in prh (orange; false discovery rate < 25%, nominal p value < 0.01). F, Enrichment plot of major types of microglia gene sets identified the positive enrichment of microglial genes in prh compared with WT.

  1. The Journal of Neuroscience vol. 42 no. 9 1820-1844
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