Mathias Khiany, Machado Richard Simon, Cardoso Taise, Naspolini Beatriz, Prophiro Josiane, Petronilho Fabricia
Laboratory of Experimental Neurology, Health Sciences Unit, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciuma, SC, Brazil.
Health Sciences Unit, Program in Health Sciences, University of South Santa Catarina, Tubarao, SC, Brazil.
Neuromolecular Med. 2025 Apr 8;27(1):25. doi: 10.1007/s12017-025-08851-3.
Neonatal hypoxic-ischemic (HI) injury is a critical condition associated with significant acute brain damage and long-term neurological impairments. Growing evidence highlights the role of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, a key multiprotein complex driving neuroinflammation, in the progression of neonatal HI brain injury. Activation of the NLRP3 inflammasome triggers the release of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), which plays a pivotal role in exacerbating brain damage. This article examines current research to better understand the relationship between neonatal HI, NLRP3 inflammasome activation, and neuroinflammatory process. Furthermore, it emphasizes the therapeutic potential of targeting this pathway, proposing its modulation as a promising neuroprotective strategy to reduce neuroinflammation and improve outcomes in affected neonates.
新生儿缺氧缺血性（HI）损伤是一种严重的病症，与显著的急性脑损伤和长期神经功能障碍相关。越来越多的证据表明，NOD样受体家族含pyrin结构域3（NLRP3）炎性小体在新生儿HI脑损伤的进展中起关键作用，NLRP3炎性小体是驱动神经炎症的关键多蛋白复合物。NLRP3炎性小体的激活会触发促炎细胞因子的释放，包括白细胞介素-1β（IL-1β），IL-1β在加重脑损伤中起关键作用。本文探讨了当前的研究，以更好地理解新生儿HI、NLRP3炎性小体激活和神经炎症过程之间的关系。此外，本文强调了针对这一途径的治疗潜力，提出调节该途径是一种有前景的神经保护策略，可减少神经炎症并改善受影响新生儿的预后。
