Slides were photographed for green and red fluorescence with a fluorescent microscope. Statistical significance was established using Kruskal Wallis test, and Dunns method was employed for post hoc comparisons. Continuous data were presented as means standard error of the mean. Neuroinflammation, blood brain barrier damage and cell apoptosis in association with cerebral white matter injury in rat hdac1 inhibitor pups after lipopolysaccharide sensitized hypoxicischemia On P11, Nissl staining showed no major injury in the cerebral cortex after LPSsensitized HI on P2. In contrast, major white matter damage was found as shown by marked decreases of MBP term and increases of GFAP in the ipsilateral hemisphere of the LPS HI group but not of the NS HI group. A day after injury on P2, the LPS HI had substantial increases of ED1 positive activated microglia, Infectious causes of cancer TNF expression, IgG extravasation and cleaved caspase 3 positive cells in the white matter set alongside the control group. These findings suggested up-regulation of neuro-inflammation, BBB disruption and cell apoptosis within the P2 rat pup type of selective white matter damage induced by LPS HI. Early and sustained JNK activation within the microglia, endothelial cells and oligodendrocyte progenitors of the white matter after lipopolysaccharide sensitized hypoxicischemia Immunoblotting analyses of ipsilateral white matter demonstrated increased JNK phosphorylation at 24 h after LPS, while JNK activation occurred early at 1 h, peaked at 6 h and persisted at 24 h post insult in the LPS HI group. Immunohistochemical analyses confirmed that the LPS HI group had increases of p JNK immunoreactivities in the Imatinib ic50 white matter at 6 and 24 h postinsult compared to the control group. Further immunofluorescence studies showed upregulated p JNK term in the ED1 positive activated microglia, RECA positive vascular endothelial cells and O4 positive oligodendrocyte progenitors in the white matter at 6 h and 24 h post insult. The activated ED1 positive microglia showed nuclear translocation of p c Jun, the downstream sign molecule of p JNK, and also highly expressed TNF 24 h post insult. Characteristically, there have been numerous p JNK positive cells mounted on or found around the microvessels within the white matter. More over, most of the g JNK good cells corp indicated cleaved caspase 3. Both vascular endothelial cells and oligodendroglial progenitor cells also denver indicated cleaved caspase 3, revealing these cells underwent apoptosis. These findings suggested the apoptosis of endothelial cells, and involvement of JNK activation in neuro-inflammation and oligodendroglial progenitors in the white matter after LPS HI damage.