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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Central activation of the fatty acid sensor GPR120 suppresses microglia reactivity and alleviates sickness- and anxiety-like behaviors

Fig. 1

Central GPR120 expression and microglial anti-inflammatory function. A Distribution of GPR120 (free fatty acid receptor 4, Ffar4) mRNA in mouse brain (whole: whole brain, NAc: nucleus accumbens, DS: dorsal striatum, Amy: amygdala, Hippo: hippocampus, PFC: prefrontal cortex, Hypo; hypothalamus) (n = 3–5/group). B GPR120 mRNA expression in primary murine microglia (MG), neurons (Neu), and astrocytes (Ast) (n = 5). C GPR120 mRNA expression in human fetal microglia (MG), neurons (Neu), and astrocytes (Ast) (n = 3–4). Effect of GPR120 agonism on D Ffar4 and E Iba-1 mRNA expression on LPS-stimulated primary microglia (n = 6–11/group). Proinflammatory cytokine mRNA expression on LPS-stimulated primary cultured microglia pre-treated with F CpdA or G unsaturated FAs (OA; oleic acid, ALA; α-linolenic acid, EPA; eicosapentaenoic acid, DHA; docosahexaenoic acid). H Cytokine protein levels in culture medium (n = 3–5/group). I Representative image of NFκB translocation after LPS-treatment with or without CpdA pre-treatment. Scale bar, 20 µm. NFκB intensity in J nuclear and K cytoplasmic compartments. L Ratio of nuclear/cytoplasmic NFκB (n = 63, from 3 cover slips). Data are expressed as the mean ± SEM. One-way ANOVA with post hoc Sidak multiple comparison test; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001 vs Veh LPS

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