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Figure 2 | Journal of Neuroinflammation

Figure 2

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 2

Upregulation of JNK activation in lipopolysaccharide-sensitized hypoxic-ischemic white matter injury. (A) Immunoblotting of white matter in the lipopolysaccharide (LPS) + hypoxic-ischemic (HI) group showed there was an early rise of phospho-c-Jun N-terminal kinase (p-JNK) expression at 1 h, which peaked at 6 h and persisted at 24 h post-insult. The JNK expression did not differ between the control and LPS + HI groups at various time points post-insult. (B) p-JNK immunohistochemistry at 6 and 24 h post-insult showed the LPS + HI group (n = 10) had significantly higher p-JNK immunoreactivities in the white matter of the ipsilateral hemisphere than the control (n = 7) groups. Scale bar =100 μm in (B). Values are means ± SEM. ***P < 0.001, **P < 0.01.

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