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目的探讨头孢曲松对大鼠弥漫性轴索损伤后海马CA1区神经元凋亡的影响。方法选择雄性Wistar大鼠120只,随机分为药物干预组(n=36):制作弥漫性轴索损伤模型,于制作模型后即刻给予头孢曲松200 mg·kg-1。假手术组(n=36):仅行头皮切开缝合处理,给予等量生理盐水腹腔注射。脑损伤组(n=36):制作弥漫性轴索损伤模型,给予等量生理盐水腹腔注射。正常对照组(n=12):不给予任何干预措施。采用免疫组化技术检测干预后12、24和36h时相海马CA1区凋亡蛋白酶激活因子-1(Apaf-1)蛋白的表达水平。结果脑损伤组和药物干预组大鼠海马CA1区Apaf-1蛋白表达水平均于12 h开始增加,24 h达高峰,此后逐渐下降。药物干预组大鼠海马CA1区Apaf-1蛋白表达水平在各个时相点均低于脑损伤组,均差异有统计学意义。结论弥漫性轴索损伤可引起大鼠海马CA1区神经元凋亡,头孢曲松可改善凋亡的发生、发展。
Objective To investigate the effect of ceftriaxone on neuronal apoptosis in hippocampal CA1 after diffuse axonal injury in rats. Methods One hundred and twenty male Wistar rats were randomly divided into drug intervention group (n = 36): The model of diffuse axonal injury was made. Ceftriaxone 200 mg · kg-1 was given immediately after the model was made. Sham operation group (n = 36): scalp incision suture only, giving the same amount of saline intraperitoneal injection. Brain injury group (n = 36): The model of diffuse axonal injury was made, and an equal volume of normal saline was injected intraperitoneally. Normal control group (n = 12): No intervention was given. Immunohistochemistry was used to detect the expression of Apaf-1 protein in hippocampal CA1 region at 12, 24 and 36 h after intervention. Results The levels of Apaf-1 protein in hippocampal CA1 region of rats in traumatic brain injury group and drug-treated group both increased at 12 h and peaked at 24 h, then decreased gradually. The level of Apaf-1 protein in hippocampal CA1 region of rats in the drug-treated group was lower than that of the brain injury group at each time point, and the difference was statistically significant. Conclusion Diffuse axonal injury can induce neuronal apoptosis in CA1 area of hippocampus, and ceftriaxone can improve the occurrence and development of apoptosis.