摘要
目的研究阿米替林(Ami)对缺氧缺糖培养大鼠脑皮层神经细胞的保护作用。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、丙二醛和超氧化物歧化酶的含量变化,观察缺氧缺糖对神经细胞的损伤及Ami的保护作用。结果缺氧缺糖引起神经细胞明显损伤性变化,死亡率升高.培养上清液中乳酸脱氢酶、一氧化氮含量升高.细胞匀浆中丙二醛生成增加.超氧化物歧化酶含量明显减少。Ami10^-7~10^-5mol/L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,机制可能与抗脂质过氧化及钙拮抗作用有关。
Objective To study the protective effects of amitriptyline (Ami ) on ischemic injury in cultured rat cerebral cortical neurons. Methods Cortical neurons of fetal rat were cultured in vitro. The effect that Ami prevent the injury of hypoxia/hypoglycemia and toxicity of Glu in cultured rat cerebral cortical neurons were observed. Results Ami ( 10^-7 ,10^-6 ,10^-5mol/L) reduced the number of cell death and lowered LDH, NO, MDA content and increase of activity of SOD. Conclusion The results suggest that Ami protected rat cerebral cortical neurons from ischemic injury. And it may attribute its to antioxidation and calcium antagonism.
出处
《滨州医学院学报》
2006年第4期247-249,共3页
Journal of Binzhou Medical University