Figure 1

Upregulation of neuroinflammation, blood–brain barrier damage and cell apoptosis in association with white matter injury in P2 rat pups after lipopolysaccharide-sensitized hypoxic-ischemia. On P11 in the LPS + HI group, Nissl staining (A) showed no significant injury in the cortex (gross picture in the upper panel; microscopic picture in the lower panel photographed from the cortex marked with an asterisk). (B) Immunohistochemical staining demonstrated that the LPS + HI group had markedly decreased MBP expression and increased GFAP-positive astrogliosis in the white matter of the ipsilateral hemisphere compared to the control and NS + HI groups. (C) Immunohistochemistry 24 h post-insult showed that the LPS + HI but not the NS + HI group had significant increases in ED1-positive microglia, TNF-α immunoreactivities, IgG extravasation, and cleaved caspase 3-positive apoptotic cells in the white matter. Microscopic pictures of (B,C) were taken from the white matter area marked with a circle in (A). ED1, microglia marker; GFAP, glial fibrillary acidic protein; HI, hypoxic-ischemia; LPS, lipopolysaccharide; MBP, myelin basic protein; NS, normal saline; P, postpartum. Scale bar = 200 μm for MBP, 50 μm for cleaved caspase 3, and 100 μm for the others.