JNK hyperactivation in the oligodendrovascular model post insult may lead to white matter injury through upregulation of neuroinflammation, blood brain barrier dysfunction and oligodendrocyte progenitor apoptosis. Abbreviations BBB: Blood-brain barrier, ED1: Microglia sign, GFAP: Glial fibrillary acidic protein, HI: Hypoxic ischemia, Ig: Immunoglobulin, IOD: Integral Bosutinib SRC inhibitor optical density, JNK: c Jun N terminal kinases, LPS: Lipopolysaccharide, MBP: Myelin basic protein, NS: Normal saline, ODN: Oligodeoxynucleotides, P: Postpartum, PBS: Phosphate buffered saline, p JNK: Phospho c Jun N terminal kinases, RNS: Reactive nitrogen species, ROS: Reactive oxygen species, TNF: Tumefaction necrosis factor. Competing interests The authors declare that they have no competing interests. Figure 10 c Jun N terminal kinase antisense oligodeoxynucleotide notably attenuated white matter injury. White matter injury Skin infection is the main type of brain injury in very pre-term infants. . Selective white matter damage in the immature brain could be induced by lipopolysaccharide sensitized hypoxic ischemia in the post-partum day 2 rat pups whose brain maturation status is equivalent to that in pre-term infants less than 30 weeks of gestation. Neuroinflammation, blood-brain barrier damage and oligodendrocyte progenitor apoptosis may possibly influence the vulnerability of LPS sensitized HI in white matter damage. c Jun N terminal kinases are essential stress responsive kinases in several types of insults. We hypothesized that LPS sensitized HI causes white matter damage through JNK activation mediated oligodendroglial apoptosis and neuro-inflammation, BBB leakage within the white matter of P2 rat pups. P2 dogs received LPS or normal saline injection followed by 90 min HI. Immunoblotting and immunohistochemistry were used to find out microglia service, TNF, BBB injury, cleaved Fostamatinib clinical trial caspase 3, , myelin basic protein, and glial fibrillary acidic . expression protein JNK and phospho JNK. Immunofluorescence was performed to determine the cellular distribution of p JNK. Genetic and pharmacological approaches were used to inhibit JNK activity. P2 puppies had selective white matter damage related to upregulation of IgG extravasation, TNF, activated microglia and oligodendroglial progenitor apoptosis after LPS sensitized HI. Immunohistochemical analyses showed early and sustained JNK activation within the white matter at 6 and 24 h post insult. Immunofluorescence demonstrated up-regulation of p JNK in activated microglia, vascular endothelial cells and oligodendrocyte progenitors, and also showed perivascular region of p JNK positive cells round the ships 24 h post insult. JNK inhibition by AS601245 or by antisense oligodeoxynucleotides dramatically paid down microglial service, TNF immunoreactivity, IgG extravasation, and cleaved caspase 3 within the endothelial cells and oligodendrocyte progenitors, and also attenuated perivascular aggregation of p JNK positive cells 24 h post insult.