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. 2015 Jun 26;138(11):3299–3315. doi: 10.1093/brain/awv172

Figure 6.

Figure 6

Candesartan and telmisartan reduce microglial activation after CCI injury. Mice were injured by CCI, treated 1 h post-injury with either PPARγ antagonist (2 mg/kg, T0070907) or vehicle, and administered vehicle, telmisartan (1 mg/kg) or candesartan (0.1 mg/kg) at 6 h post-injury, then daily until sacrifice at 3 days post-injury. (A) Representative images from brain sections from perilesional cortex at −1.70 mm from Bregma immunostained with Iba-1 antibody. Five fields per brain section were counted. Scale bar = 500 μm. (B–G) CCI-induced increases in microglial (Iba-1+) density and hypertrophic morphology in vehicle-treated mice (B) were reduced by candesartan (C) or telmisartan (D) treatments. The PPARγ antagonist enhanced CCI-induced microglia activation (E) and partially decreased the candesartan (F) and telmisartan protective effects (G). Small inset images (b–g) are magnified to reveal details of the hypertrophic/bushy activated microglial cells. Scale bars for B–G = 50 μm; b–g = 20 μm. (H) Quantitative analysis of the density of Iba-1+ cells for each group. Data are means ± SEM, n = 5–12. **P < 0.01, ***P < 0.001 candesartan, or telmisartan versus vehicle; #P < 0.05, ##P < 0.01, ###P < 0.001, PPARγ antagonist treatment versus same treatment group without antagonist. (I and J) Candesartan and telmisartan reduce lipopolysaccharide-induced inflammatory gene expression in primary microglia. Primary microglia were treated with candesartan or telmisartan for 2 h before addition of lipopolysaccharide (LPS, 10 ng/ml) for 12 h before harvesting. QPCR analysis shows (I) iNOS (Nos2) and (J) IL-1β (Il1b) mRNA expression in different conditions. Data are mean ± SEM, n = 4–8. ****P < 0.0001, ***P < 0.001, *P < 0.05 treatments versus lipopolysaccharide alone.