A selective white matter damage model in P2 rat pups induced by lipopolysaccharide sensitized hypoxicischemia. Much like the construction 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 main target of white matter price Dovitinib injury in the preterm infants. All through detrimental insults within the immature brain, activated microglia may exacerbate white matter damage through generation of pro inflammatory cytokines, such as TNF. The damaged microvessels may hire activated leukocytes into the hurt white matter through the damaged BBB, resulting in sustained activation of the white matter is further damaged by microglia, which in turn through production of inflammatory cytokines. Because microglia, vascular endothelial cells and oligodendrocytes may directly connect to one another in the white matter, there may be considered a common signaling mechanism connecting neuro-inflammation, BBB disruption and oligodendroglial progenitor cell apoptosis in the Plastid white matter injury of the immature brain. D Jun N terminal kinases are important stressresponsive kinases that are triggered by various kinds of insults, including ischemia. JNK initial precedes cell death by inflammation and apoptosis in several cell types. Activation of JNK signaling leads not just to pro inflammatory cytokine production, but in addition to cell death via intrinsic/extrinsic apoptotic pathways. In vitro studies show that JNK signaling is the prevalent route for cytokine generation from LPSstimulated or hypoxia exposed microglia. JNK signaling Foretinib solubility also plays an important part in subarachnoid hemorrhage associated BBB disruption, and stressinduced apoptosis of oligodendrocyte progenitors and cerebral endothelial cells. In vivo studies demonstrated early and lasting JNK initial after cerebral ischemia. Our previous study in P7 rat pups showed that neonatal obese improved HI induced microglial activation, neuronal apoptosis and BBB damage in the cerebral cortex, and annoyed cortical damage through JNK hyperactivation. However, it remains uncertain whether JNK activation will be the common pathogenic mechanism within the oligodendrovascular unit ultimately causing white matter damage in the immature mind of P2 rat pups. Using an established model 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 damage 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 using a 12/12 h light/dark period.