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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Hippocampal microRNA-26a-3p deficit contributes to neuroinflammation and behavioral disorders via p38 MAPK signaling pathway in rats

Fig. 7

The p38/NF-κB/NLRP3 pathway mediated the miR-26a-3p deficiency-induced neuronal dysfunction. A Immunofluorescent staining showed Iba-1-positive microglia. B The number of Iba-1-positive microglia within the hippocampal region was decreased after daily treatment with SB203580 for 2 weeks in miR-26a-3p knock-down rats. C The microglia showed the resting states after the daily treatment with SB203580 for 2 weeks in miR-26a-3p deficiency rats. D SB203580 treatment reduced the increased phosphorylated level of p65 and expression level of NLRP3 induced by knock-down of miR-26a-3p. E–G SB203580 treatment reduced the increased level of IL-1β, IL-6 and IFN-γ induced by knock-down of miR-26a-3p. H, I SB203580 treatment has increased levels of IL-4 and IL-10 reduced by knock-down of miR-26a-3p. J Raw traces of sEPSC by patch-clamp recordings. K SB203580 treatment reversed the decreased amplitude of sEPSC. L SB203580 treatment reversed the decreased frequency of sEPSC. Data are presented as the means ± SEMs. N = 6–8 per group. For electrophysiological recordings, N = 6 neuros from 4 rats per group. *P < 0.05, **P < 0.01, ***P < 0.001

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