期刊
PEDIATRIC RESEARCH
卷 68, 期 1, 页码 41-47出版社
NATURE PUBLISHING GROUP
DOI: 10.1203/PDR.0b013e3181df5f6b
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- Taiwan National Health Research Institute [NHRI-EX 97-9414NI]
- National Science Counsel (NSC) [97-2811-B-006-014]
- Chi Mei Medical Center [CMNCKU 9802]
- Center for Gene Regulation and Signal Transduction Research, National Cheng Kung University
Little is known about roles of inflammation and hypoxic ischemia (HI) in the generation of neuroinflammation and damage of blood-brain barrier (BBB) in the white matter (WM) that displays regional vulnerability in preterm infants. We investigated whether low-dose lipopolysaccharide (LPS) sensitizes HI-induced WM injury in postpartum (P) day 2 rat pups by selectively increasing neuroinflammation and BBB damage in the WM. Pups received LPS (0.05 mg/kg) (LPS + HI) or normal saline (NS + HI) followed by 90-min HI. LPS and NS group were the pups that had LPS or NS only. Myelin basic protein immunohistochemistry on P11 showed WM injury in LPS + HI group, but not in NS + HI, LPS, and NS groups. In contrast, no gray matter injury was found in the four groups. LPS + HI group also showed decreased number of oligodendrocytes in the WM 72-h postinsult. In the same brain region, increases of activated microglia, TNF-alpha expression, BBB leakage, and cleaved caspase-3 positive cells were much more prominent in LPS + HI group than in the other three groups 24-h postinsult. The oligodendrocytes were the major cells with cleaved caspase-3 expression. We concluded that low-dose LPS sensitized HI-induced WM injury in the immature brain by selectively up-regulating neuroinflammation and BBB damage in the WM. (Pediatr Res 68: 41-47, 2010)
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