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Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

LPS-sensitized HI caused selective white matter injury. P2 rat pups received LPS (0.05 mg/kg) or NS 3 h before 90 min of HI. Neuropathological tests were performed on P12 (a, left panel). Nissl staining revealed no significant injury in the gray matter of the control (n = 6), NS + HI (n = 6), and LPS + HI (n = 6) groups. Upper panel: brain section at the level of striatum (0.26 mm posterior to the bregma) and lower panel: the section at the level of dorsal hippocampus (3.14 mm posterior to the bregma). The LPS + HI group had significantly higher ipsilateral ventricular size ratios (a, right panel), lower myelination (MBP) (b), and higher astrogliosis (GFAP) (c) in the white matter than those of the control group. Scale bar = 100 μm for MBP and GFAP. Values are means ± SEMs. **p < 0.01. Values are means ± SEMs. NS, normal saline; LPS, lipopolysaccharide; HI, hypoxic ischemia; MBP, myelin basic protein; GFAP, glial fibrillary acidic protein

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