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Figure 4 | Journal of Neuroinflammation

Figure 4

From: TNFR1-JNK signaling is the shared pathway of neuroinflammation and neurovascular damage after LPS-sensitized hypoxic-ischemic injury in the immature brain

Figure 4

Up-regulation of c-Jun N-terminal kinase (JNK) activation in microglia, endothelial cells, neurons, and oligodendrocyte progenitors after lipopolysaccharide (LPS)-sensitized hypoxic-ischemia (HI). (A) Immunoblotting showed that the LPS + HI group (n = 4), but not the NS + HI group (n = 4) had increased p-JNK expression at 6 and 24 hours post-insult compared to the control group (n = 3). (B) Immunofluorescence in the LPS + HI group 24 hours post-insult showed up-regulation of p-JNK expression in Iba1-positive microglia, IB4-positive microvascular endothelial cells, NeuN-positive neurons, and O4-positive oligodendrocyte progenitors. Arrowheads indicate many p-JNK-positive cells attached to or were located around the IB4-positive microvessels. Scale bar = 50 μm for Iba1 and IB4, and 25 μm for others. Inset scale bar = 2.5 μm. Values are means ± SEM. *P < 0.05, ***P < 0.001.

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