Figure 7

Tumor necrosis factor receptor 1 (TNFR1) deficiency reduced c-Jun N-terminal kinase (JNK), microglial activation and blood–brain barrier (BBB) damage, and attenuated injury after lipopolysaccharide (LPS)-sensitized hypoxic-ischemia (HI). (A) At 24 hours post-insult, the TNFR1- (n = 12) but not the TNFR2-KO (n = 12) pups had significant reduction in p-JNK expression and decreased Iba1-positive microglia, IgG extravasation, and cleaved caspase 3-positive cells than the WT pups (n = 10). (B) The TNFR1-KO but not the TNFR2-KO mice also had significantly reduced cortical injury (Nissl stain, upper panel), preserved myelination (MBP, middle panel), and decreased astrogliosis (GFAP, lower panel) than the WT mice on P17. GFAP, glial fibrillary acidic protein; Iba-1, ionized calcium-binding adaptor molecule-1; KO, knockout; MBP, myelin basic protein; WT, wild-type. Scale bar = 100 μm in (A), and 200 μm for MBP, 100 μm for GFAP in (B). Inset scale bar = 10 μm. Values are means ± SEM. ***P < 0.001, **P < 0.01, *P < 0.05.