目的 探讨头孢曲松对新生大鼠缺氧缺血性脑损伤（HIBD）的保护作用，并考察其作用机制。方法 新生SD大鼠随机分为假手术组、模型组和头孢曲松组，每组各48只，各组依据造模成功后观察时间点又分为6 h、12 h、24 h、3 d、5 d、7 d 6个亚组，每个亚组各8只。假手术组只做颈部切开和右颈总动脉分离术，不结扎。模型组、头孢曲松组均制备新生大鼠HIBD模型。假手术组、模型组于术后ip生理盐水10 mL/kg，1次/d，连续3 d；头孢曲松组于术后ip注射用头孢曲松钠200 mg/kg，1次/d，连续3 d。热板法测试记录新生大鼠热板测试时间；HE染色后观察皮质脑组织病理变化；Westernblotting法测定FADD表达量；免疫组化法检测FADD阳性表达细胞数。结果 与模型组比较，头孢曲松组的热板测试时间在3、5 d时明显缩短，差异具有统计学意义（P<0.05）。通过光学显微镜观察发现头孢曲松组脑组织细胞排列尚规则，体积稍大，呈轻度水肿改变。与模型组比较，头孢曲松组在各个时间点的FADD表达量和阳性表达细胞数明显降低（P<0.05）。结论 头孢曲松可下调HIBD新生大鼠脑皮质FADD表达，减少凋亡发生，改善行为学表现，发挥神经保护作用。

Objective To study the protective effect of ceftriaxone against hypoxic-ischemic brain injury in neonatal rats, and investigate its mechanism. Methods Neonatal SD rats were randomly divided into Sham group, model group, and ceftriaxone group, and each group was divided into 6 h, 12 h, 24 h, 3 d, 5 d, and 7 d subgroup with 8 rats according to observation time. Rats in the Sham group were performed only by incision of neck and right common carotid artery dissection without ligation. Rats in the ceftriaxone group and model group were successfully established hypoxic ischemic brain damage (HIBD) models. Rats in the Sham group and model group were ip administered with normal saline after the operation, 10 mL/kg, once daily, treated for 3 d. Rats in the ceftriaxone group were ip administered with Ceftriaxone Sodium for injection after the operation, 200 mg/kg, once daily, treated for 3 d. Hot plate test method was used to record hot plate test time in neonatal rats. HE staining was used to observe the pathological changes of cortex. FADD expression was detected by Western blotting method. The number of FADD positive cells was detected by immunohistochemical staining. Results Compared with the model group, hot plate test time in the ceftriaxone group were significantly shorter on days 3 and 5, and there were differences between two groups (P<0.05). By optical microscope observation, brain tissue cell arrangement in ceftriaxone group was still rule, the volume slightly larger, and a slight edema changes. Compared with the model group, FADD expression and positive cells numbers in the ceftriaxone group were obviously decreased at various time points, (P<0.05). Conclusion Ceftriaxone can down-regulate FADD expression in cerebral cortex of neonatal rats with HIBD, reduce neuron cell apoptosis, improve behaviors, and play neuroprotective effect.