In vitro kinase assay of h Jun N terminal kinase within the lipopolysaccharide hypoxic ischemic group showed that AS601245 successfully blocked JNK activity at 6 and 24 h post insult compared with vehicle. k63 ubiquitin Immunofluorescent staining in the lipopolysaccharide hypoxic ischemic team showed that, in contrast to automobile, AS601245 somewhat attenuated perivascular phospho c Jun N terminal kinase positive cell attachment, and also lowered cleaved caspase 3 positive endothelial and oligodendroglial cells in the white matter. In addition to cell death, enduring oligodendrocyte progenitors might be discouraged from differentiation and proliferation by reactive astrocytes and microglial activation. Our results of reactive astrogliosis and hypomyelination on P11 after LPS HI resembled the results of impairment and neuroinflammation of oligodendroglial maturation. The compound or signaling pathway that leads to JNK activation within the oligodendrovascular system of the white matter in the immature brain remains unclear. Common to both ischemia and infection may be the generation of reactive oxygen and nitrogen species, particularly nitric oxide. Nitric oxide mRNA production in excess could be negative, particularly in the presence of ROS, that are known to be connected with oligodendrocyte death and white matter damage in pre-term infants. . Autopsy studies in pre-term infants with periventricular white matter damage have demonstrated lipid peroxidation and protein nitration in pre myelinating oligodendrocytes. An animal experiment showed the free radical scavenging Celecoxib structure adviser N acetylcysteine effectively protected against LPS sensitized HI brain damage in neo-natal rats. . These findings suggest a role for ROS/RNS in the pathogenesis of white matter damage. Studies also have demonstrated the synergistic effect of HI and LPS activated microglia to make ROS/RNS, resulting in continuous JNK activation which often facilitated TNF synthesis and more ROS/RNS accumulation in a positive feedback loop. These reports confirmed that JNK signaling is an integral modulator in cell death mediated by ROS/ RNS. Triggered microglia might use cytotoxicity to endothelial cells and donate to BBB break-down and oligodendrocyte progenitors through both JNK TNF and ROS/RNS trails. The pre myelinating oligodendrocytes are specially more vulnerable to oxidative and nitrosative harm than mature oligodendrocytes due to reduced antioxidant defenses and susceptibility to glutamate excitotoxicity. Joyful expression of calciumpermeable glutamate receptors and over-expression of glutamate transporters within the immature brain give rise to the dependent vulnerability of pre myelinating oligodendrocytes to glutamate excitotoxicity.