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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Clemastine improves hypomyelination in rats with hypoxic–ischemic brain injury by reducing microglia-derived IL-1β via P38 signaling pathway

Fig. 1

aw show interleukin-1beta (IL-1β) and nod-like receptor protein 3 (NLRP3) protein expression levels in the corpus callosum of rats at 1, 3, and 7 days after the bilateral common carotid artery occlusion (BCCAO) and clemastine injection after BCCAO when compared with their corresponding controls. Double immunofluorescence staining showing the distribution of Iba-1-labeled (a, d, g, k, n, and q, green) and IL-1β (b, e, and h, red) and NLRP3 (l, o, and r, red) immunoreactive amoeboid microglial cells (AMCs) in the corpus callosum of rats at 1 day after BCCAO and clemastine injection after BCCAO and their corresponding controls. The colocalized expression of Iba-1 and IL-1β or NLRP3 in AMCs can be seen in c, f, l, or m, p, s. Bar graphs (j and t) depict remarkable increases in the immunofluorescence intensity of IL-1β and NLRP3 expression levels, following BCCAO challenge when compared with matched controls; clemastine reversed these changes. Panel U shows IL-1β (17 kDa), NLRP3 (62 kDa), and β-actin (42 kDa) immunoreactive bands. Panels V and W show bar graphs depicting significant increases in the optical density of IL-1β and NLRP3 after BCCAO when compared with their corresponding controls. Meanwhile, clemastine could remarkably decrease the expression of IL-1β and NLRP3 at 1day. N = 3. *P < 0.05. Scale bars: A–S 50 μm

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