阿米替林对缺血损伤神经元bcl-2和bax表达的影响  

Effects of amitriptyline on expression of bcl-2 and bax in rats neurons after anoxia

作　　者：路永辉[1] 胡营滨[2] 许勇[3] 

机构地区：[1]滨州医学院,滨州市256603 [2]滨州医学院附属医院消化内科 [3]滨州医学院药理学教研室,滨州市256603

出　　处：《滨州医学院学报》2008年第4期267-269,共3页Journal of Binzhou Medical University

摘　　要：目的研究阿米替林（Ami）对缺血损伤神经元bcl-2和bax表达的影响。方法分离培养15—18d胎龄的大鼠神经细胞，用连二亚硫酸钠消除培养基中的氧合并培养基缺糖模拟细胞缺血性损伤，测定乳酸脱氢酶、一氧化氮、谷胱甘肽过氧化物酶的含量变化，观察缺氧缺糖对神经细胞的损伤及Ami的保护作用，并使用Hoechst33342荧光染色法、免疫细胞化学染色法观察Ami对原代神经细胞的抗凋亡作用。结果缺氧缺糖引起神经细胞明显损伤性变化，存活率下降，凋亡率升高，培养上清液中乳酸脱氢酶、一氧化氮含量升高，谷胱甘肽过氧化物酶水平显著降低，促进缺氧神经细胞产生bcl-2，并减少bax的产生。Ami10^-7 - 10^-5mol·L^-1能不同程度地减轻上述损伤性变化。结论Ami对神经细胞“缺血”性损伤有保护作用．其抗凋亡机制可能与增加bcl-2表达，下调bax表达有关。Objective To study the effects of amitriptyline （Ami） on expression of bcl-2 and bax in rats neurons after anoxia. Methods The injury model of cultured neurons was made by the administration of sodium dithionite and glucose-deprived Earle＇s solution. The protective effects of Ami in vitro analyzed with MTT reduction assay was observed by determining the content of nitric oxide （NO）by Griess reagent and the activities of lactate dehydrogenase（LDH） and glutathione peroxidase （eGSH-Px）by LDH and GSH-Px kits, respectively. The anti-apoptosis effect of Ami on primary cultured neurons was observed by methods of Hoechst 33342 staining and immunocytochemistry. Results Ami （ 10^-7 ,10^-6 ,10^-5 mol · L^-1 ） dropped apoptosis rate of cerebral cortical neurons induced by hypoxia, increased bcl-2 protein expression and decreased bax protein expression. Conclusion The results suggest that Ami is able to prevent hypoxic neurons from apoptosis in primary cultured cerebral cortical neurons. The effect of anti-apoptosis is through up-regulation of bcl-2 protein expression and down-regulation of bax protein expression.

关 键 词：阿米替林 神经细胞 缺氧 凋亡 

分 类 号：R338[医药卫生—人体生理学]