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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: CXCL5 signaling is a shared pathway of neuroinflammation and blood–brain barrier injury contributing to white matter injury in the immature brain

Fig. 5

Pharmacological inhibition of CXCR2 significantly attenuated microglial activation and BBB damage and protected against white matter injury after LPS-sensitized HI. A selective nonpeptide inhibitor of CXCR2, SB22 5002, was used to examine the role of the CXCL5–CXCR2 pathway in white matter injury after LPS-sensitized HI. After LPS + HI on P2, the SB-3 group (n = 9), but not the SB-1 group (n = 7), had significantly reduced ipsilateral ventricular size ratios (a), increased myelination (MBP) (b), and reduced astrogliosis (GFAP) (c) in the white matter on P12 compared with the vehicle-treated pups (n = 9). Scale bar = 100 μm. The SB-3 group (n = 9), but not the SB-1 group (n = 7), had a significantly reduced number of activated microglia (ED1) (d) and significantly lower BBB damage (IgG extravasation) (e) in the white matter compared with the vehicle group (n = 9) at 24 h after HI. Scale bar = 50 μm (ED1) and 100 μm (IgG); values are means ± SEMs, **p < 0.01

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