一氧化氮介导新生鼠窒息缺氧引起的脑损伤

Nitric Oxide Mediates Brain Injury Induced by Perinatal Asphyxia in Neonatal Mice

摘要: 观察了新生小鼠窒息缺氧后一氧化氮（NO）水平和一氧化氮合酶（NOS）活性的变化。结果显示,新生小鼠经25min窒息缺氧,48h后脑组织NO水平、总NOS活性、iNOS和cNOS活性均显著升高,表明新生小鼠窒息缺氧可通过诱导iNOS和激活cNOS产生过量NO导致脑损伤。结果还显示,于窒息缺氧后24h腹腔注射iNOS选择性抑制剂氨基胍,可抑制iNOS活性,从而防止NO过量产生,提示iNOS抑制剂对治疗新生儿窒息缺氧引起的脑损伤有潜在应用价值。

Abstract: Effect of asphyxia on nitric oxide (NO) content and nitric oxide synthase (NOS) activity in the brains of neonatal mice was studied in this paper. Neonatal mice were subjected to asphyxia for 25 min. At 48 h after asphyxia, NO content, total NOS activity,