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Figure 6 | Journal of Neuroinflammation

Figure 6

From: JNK signaling is the shared pathway linking neuroinflammation, blood–brain barrier disruption, and oligodendroglial apoptosis in the white matter injury of the immature brain

Figure 6

AS601245 significantly reduced neuroinflammation, blood–brain-barrier damage and cell apoptosis after lipopolysaccharide-sensitized hypoxic-ischemic white matter injury. (A) In vitro kinase assay of c-Jun N-terminal kinase (JNK) in the lipopolysaccharide (LPS) + hypoxic-ischemic (HI) group showed that AS601245 (40 mg/kg) effectively blocked JNK activity at 6 and 24 h post-insult compared with vehicle. (B) AS601245 (40 mg/kg) treatment (n = 8) significantly reduced upregulation of ED1-positive activated microglia, TNF-α immunoreactivities, IgG extravasation and cleaved caspase 3-positive cells in the white matter 24 h post-insult compared to vehicle (n = 7). Scale bar =100 μm for ED1, TNF-α and IgG; 50 μm for cleaved caspase 3. Values are means ± SEM. ***P <0.001, **P < 0.01, *P < 0.05.

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