Neonatal hypoxic–ischemic encephalopathy is the most common cause of neurological disability in infancy. Superimposed inflammation may further worsen neurological outcomes. Reliable biomarkers which are both sensitive to hypoxic-ischemia and inflammation are critically needed. We tested plasma osteopontin (OPN) and glial fibrillary astrocytic protein (GFAP) within the reported therapeutic window (90 min after hypoxic-ischemic (HI) injury) in neonatal rats with different HI severity and inflammation. Two different HI severity groups (mild-HI with 75 min hypoxia and severe-HI with 150 min hypoxia) were established. Inflammation-sensitized HI brain injury induced by lipopolysaccharide (LPS) further increased apoptotic neurons and infarct volumes. In HI alone groups, OPN was significantly decreased (p < 0.001) but GFAP was slightly increased (p < 0.05) at 90 min after HI either in mild-HI or severe-HI compared with naïve group. In LPS-sensitized HI groups, both OPN and GFAP were significantly increased either in LPS-mild-HI or LPS-severe-HI groups compared with the naïve group (all p < 0.05). Induced inflammation by LPS exaggerated neonatal HI brain injury. The plasma OPN and GFAP levels may be useful to differentiate HI alone groups from inflammation-sensitized HI groups or naïve group.

新生儿缺氧缺血性脑病是婴儿期神经功能障碍的最常见原因。叠加的炎症可能会进一步恶化神经系统的结果。迫切需要对缺氧缺血和炎症都敏感的可靠生物标志物。我们在报告的治疗窗内（缺氧缺血性（HI）损伤后 90 分钟）在具有不同 HI 严重程度和炎症的新生大鼠中测试了血浆骨桥蛋白 (OPN) 和胶质纤维星形胶质细胞蛋白 (GFAP)。建立了两个不同的 HI 严重程度组（轻度 HI 缺氧 75 分钟和重度 HI 缺氧 150 分钟）。脂多糖 (LPS) 诱导的炎症致敏 HI 脑损伤进一步增加了凋亡神经元和梗死体积。在单独 HI 组中，OPN 显着降低（p < 0.001），但 与初始组相比，轻度 HI 或重度 HI HI 后 90 分钟GFAP 略有增加（p < 0.05）。在 LPS 致敏 HI 组中，与幼稚组相比，LPS-轻度-HI 或 LPS-重度-HI 组的 OPN 和 GFAP 均显着增加（均p  < 0.05）。致我用LPS nflammation夸张新生儿HI脑损伤。血浆 OPN 和 GFAP 水平可能有助于区分 HI 单独组与炎症敏感 HI 组或初始组。