| First Author | Micili SC | Year | 2020 |
| Journal | Neurosci Lett | Volume | 738 |
| Pages | 135389 | PubMed ID | 32949661 |
| Mgi Jnum | J:298699 | Mgi Id | MGI:6477181 |
| Doi | 10.1016/j.neulet.2020.135389 | Citation | Micili SC, et al. (2020) Oxygen exposure in early life activates NLRP3 inflammasome in mouse brain. Neurosci Lett 738:135389 |
| abstractText | Despite widely known detrimental effects on the developing brain, supplemental oxygen is still irreplaceable in the management of newborn infants with respiratory distress. Identifying downstream mechanisms underlying oxygen toxicity is a key step for development of new neuroprotective strategies. Main purpose of this study is to investigate whether NLRP3 inflammasome activation has a role in the pathogenesis of hyperoxia-induced preterm brain injury. C57BL6 pups were randomly divided into either a hyperoxia group (exposed to 90 % oxygen from birth until postnatal day 7) or control group (maintained in room air; 21 % O2). At postnatal day 7, all animals were sacrificed. Immunohistochemical examination revealed that hyperoxic exposure for seven days resulted in a global increase in NLRP3 and IL-1beta immunopositive cells in neonatal mouse brain (p</=0.001). There was a significant rise in Caspase-1 positive cell count in prefrontal and parietal area in the hyperoxia group when compared with controls (p</=0.001). Western blot analysis of brain tissues showed elevated NLRP3, IL-1beta and Caspase-1 protein levels in the hyperoxia group when compared with controls (p</=0.001). To the best of our knowledge, this is the first study that investigates an association between hyperoxia and establishment of NLRP3 inflammasome in preterm brain. |
