A selective white matter injury model in P2 rat pups induced by lipopolysaccharide sensitized hypoxicischemia. Much like the framework of the neurovascular unit in the cerebral cortex, microglia, oligodendrocyte progenitors and microvascular endothelial cells may form a closely inter-related oligodendrovascular unit in the white matter, which may be the major target of white matter Linifanib FLT-3 inhibitor injury in the pre-term infants. Throughout damaging insults in the immature mind, activated microglia may possibly exacerbate white matter injury through generation of pro inflammatory cytokines, including TNF. The broken microvessels may get activated leukocytes to the injured white matter through the damaged BBB, resulting in sustained activation of microglia, which further damage the white matter through extended production of inflammatory cytokines. Since microglia, vascular endothelial cells and oligodendrocytes may strongly interact with each other in the white matter, there may be a common signaling mechanism linking neuro-inflammation, BBB disruption and oligodendroglial progenitor cell apoptosis in the RNApol white matter damage of the immature brain. H Jun N terminal kinases are critical stressresponsive kinases that are triggered by various types of insults, including ischemia. JNK service precedes cell death by inflammation and apoptosis in several cell types. Activation of JNK signaling leads not just to cell death via intrinsic/extrinsic apoptotic pathways, but in addition to pro-inflammatory cytokine production. In vitro studies demonstrate that JNK signaling is the predominant process for cytokine manufacturing from LPSstimulated or hypoxia exposed microglia. JNK signaling BAY 11-7082 also plays an essential part in subarachnoid hemorrhage associated BBB disruption, and stressinduced apoptosis of cerebral endothelial cells and oligodendrocyte progenitors. In vivo studies demonstrated early and enduring JNK service after cerebral ischemia. Our previous study in P7 rat pups showed that neonatal chubby increased HI induced neuronal apoptosis, microglial activation and BBB damage in the cerebral cortex, and angry cortical damage through JNK hyperactivation. However, it remains unclear whether JNK activation will be the common pathogenic mechanism in the oligodendrovascular model leading to white matter injury in the immature brain of P2 rat pups. Having an established type of LPS sensitized HI white matter injury in P2 rat pups, we hypothesized that JNK signaling is the shared pathway linking neuroinflammation, microvascular endothelial cell injury and BBB breakdown, and apoptosis of oligodendroglial precursor cells in the white matter injury of the immature brain. The animal study was approved by the Animal Care Committee at National Cheng Kung University. Sprague Dawley rat pups were stored under standard condition with a 12/12 h light/dark pattern.