盐酸纳洛酮对大鼠脑神经损伤保护作用机制的研究  

Protective Mechanism of Naloxone to Nerve Cell Injury of Rat

作　　者：王丽虹[1] 许天英[2] 王晓敏[2] 李波[1] 

机构地区：[1]哈尔滨医科大学免疫教研室,黑龙江哈尔滨150086 [2]黑龙江省医院脑外科,黑龙江哈尔滨150036

出　　处：《黑龙江医学》2005年第8期591-592,共2页Heilongjiang Medical Journal

摘　　要：目的研究纳洛酮对脑神经损伤后神经细胞培养液中肿瘤坏死因子α(TNF-α)含量的测定,探讨纳洛酮对神经保护作用的机制。方法大鼠脑神经细胞培养种植于6孔板,采用平板离心损伤模型,通过ELISA双抗体夹心法检测培养液中TNF-α的水平,观察损伤后不同时间段不同组TNF-α含量变化。结果TNF-α在损伤后2h开始升高,12h达到高峰,随后有所降低,至24h趋于平缓。纳洛酮治疗组神经细胞损伤后12h、24h、48h、72hTNF-α的水平与损伤组比较有差异(P<0.05)。结论纳洛酮能够通过降低TNF-α的含量起到神经保护作用。Objective To assess the degree of axonal injury and recovery by measuring the content of TNF - a in neuron culturing liquid.Methods Neuron precursor culture and explant in culture plate applying the injury model of plate centrifuge to observe in variant time the changing of TNF-a content. The level of TNF-a was detected with ELISA. Results TNF-a began ascending after2, 12 hour get to high peek and then descend, until 24 h began mild. There was statistically difference between the trial group and injury group. Concluston Naloxone could protect nerve cell through decrease the level of TNF-α.

关 键 词：神经外科学 神经细胞 纳洛酮 肿瘤坏死因子-Α 

分 类 号：R657.1[医药卫生—外科学]