Figure 2

Lipopolysaccharide (LPS)-sensitized hypoxic-ischemic (HI) injury induced up-regulation of neuroinflammation, blood–brain barrier damage and cell apoptosis. (A) P5 mouse pups received normal saline (NS) or LPS (0.05 mg/kg) injection before 30-minute HI. Neuropathology was performed on P17. Compared to the control group (n = 6), the LPS + HI group (n = 10) but not the NS + HI group (n = 10) had significantly increased cortical damage (Nissl staining, upper panel), markedly reduced myelination (MBP, middle panel), and increased astrogliosis in the ipsilateral hemisphere (GFAP, lower panel). (B) At 24 hours post-insult, immunohistochemistry revealed that the LPS + HI group (n = 10) had significant increases in Iba1-positive microglia and IgG extravasation than the NS + HI (n = 10) and control (n = 6) groups. (C) LPS injection before HI did not up-regulate TNF-α expression compared to NS injection (upper panel). TNF-α levels were significantly increased at 3 hours, and especially at 24 hours after LPS-sensitized HI (lower panel). n = 4 experiments. (D) The LPS + HI group had significantly higher levels of TNF-α (upper panel) and cleaved caspase-3 (lower panel) than the NS + HI group at 24 hours post-insult. n = 6 experiments. Scale bar = 200 μm for MBP and = 100 μm for others. Inset scale bar = 10 μm in (B). Values are means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001. GFAP, glial fibrillary acidic protein; Iba-1, ionized calcium-binding adaptor molecule-1; MBP, myelin basic protein.