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-1β 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-1β 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.

尽管众所周知，这对发育中的大脑有害，但在处理呼吸窘迫的新生儿时，补充氧气仍然是不可替代的。确定潜在的氧气毒性下游机制是开发新的神经保护策略的关键步骤。这项研究的主要目的是调查NLRP3炎性小体活化是否在高氧引起的早产脑损伤的发病机理中起作用。将C57BL6幼犬随机分为高氧组（从出生到出生后第7天，暴露于90％的氧气）或对照组（保持在室内空气中； 21％的O _2））。在出生后第7天，将所有动物处死。免疫组织化学检查显示，高氧暴露7天导致新生小鼠脑中NLRP3和IL-1β免疫阳性细胞的总体增加（p≤0.001）。与对照组相比，高氧组的前额叶和顶叶区的Caspase-1阳性细胞计数显着增加（p≤0.001）。脑组织的蛋白质印迹分析显示，与对照组相比，高氧组的NLRP3，IL-1β和Caspase-1蛋白水平升高（p≤0.001）。据我们所知，这是第一项研究高氧与早产儿大脑中NLRP3炎性体的建立之间的关联的研究。