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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 m L/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;Western blotting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 investigate the protective effect of ceftriaxone on hypoxic-ischemic brain damage (HIBD) in neonatal rats and its mechanism of action. Methods Newborn SD rats were randomly divided into sham operation group, model group and ceftriaxone group, each group of 48, each group was divided into 6 h, 12 h, 24 h, 3 d , 5 d, 7 d 6 subgroups, each subgroup of 8. The sham-operated group only underwent neck incision and right common carotid artery dissection without ligation. Model group, ceftriaxone group were prepared neonatal HIBD model. The rats in the sham operation group and the model group were treated with ip saline 10 m L / kg once a day for 3 consecutive days. After ceftriaxone treatment, ceftriaxone sodium 200 mg / kg, once daily For 3 days. The hot plate test was used to record the time of hot plate test in neonatal rats. The histopathological changes of cerebral cortex were observed by HE staining. The expression of FADD was detected by Western blotting. The number of FADD positive cells was detected by immunohistochemistry. Results Compared with the model group, the test time of hot plate in ceftriaxone group was significantly shortened at 3 and 5 days, with statistical significance (P <0.05). Observed by light microscopy, ceftriaxone group showed regular arrangement of cells in brain tissue, slightly larger volume, showing mild edema. Compared with the model group, the amount of FADD expression and the number of positive cells in ceftriaxone group at each time point decreased significantly (P <0.05). Conclusion Ceftriaxone can down-regulate the expression of FADD in the cerebral cortex of HIBD neonatal rats, reduce the occurrence of apoptosis, improve the behavior and exert the neuroprotective effect.