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. 2016 Oct 26;36(43):10990–11005. doi: 10.1523/JNEUROSCI.1480-16.2016

Figure 2.

Figure 2.

Serum UA elevation results in chronic hippocampal neuroinflammation and gliosis. A–F, Hippocampal CA1 (A, B), CA2 (C, D), and CA3 (E, F) sections of the rats fed a standard chow or a HUAD were immunostained for GFAP (left) and Iba-1 (right). Immunofluorescence detection of the astrocytic marker GFAP protein and of the microglial marker Iba-1 in the rat hippocampus (4 μm) from rats fed either chow or a HUAD for 12 weeks. The image is displayed at 200× the original magnification and was used for the quantification of hippocampal astrocyte and microglia numbers. The mean numbers of hippocampal astrocytes and microglia in rats fed either chow or a HUAD were quantified in the regions displayed on the right (mean ± SEM; n = 6 rats per group). *p < 0.05; **p < 0.01; ***p < 0.001 vs chow-fed controls. G, Time course of the induction of mRNA expression of inflammatory mediators, including proinflammatory cytokines (Il6, Il1b, Tnfa, Socs3, and Ccl2) and TLR4/NF-κB signaling (Tlr4, Nfkbia, Ikbkb, and Ikbke) in the hippocampi of rats that were fed chow or a HUAD for up to 12 weeks (n = 6 rats per group). All mRNA species were quantified relative to the expression of the housekeeping gene Gapdh and are presented as fold changes relative to chow-fed controls. All displayed values are reported as the mean ± SEM. *p < 0.05 vs chow-fed control.