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目的:研究氧化槐定碱(oxysophoridine,OSR)对原代培养的新生大鼠海马神经元缺氧损伤的保护作用及其机制。方法:以原代培养的新生大鼠海马神经元为研究对象,用无糖培养液结合物理性缺氧建立缺氧损伤模型,测定神经细胞的存活率、乳酸脱氢酶(LDH)漏出率以及细胞中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、一氧化氮合酶(NOS)和一氧化氮(NO)水平的变化。采用荧光双波长分光光度计测定神经细胞内游离钙离子浓度([Ca2+]i)的变化。结果:缺氧损伤模型组能在短时间内造成神经元的死亡,LDH漏出率的增多,MDA,NO含量增多,NOS活性升高,SOD,GSH-PX活性降低,细胞内[Ca2+]i增加。OSR组(0.625,5,10μg.L-1)能不同程度地降低缺氧模型对神经元的损伤。结论:氧化槐定碱对新生大鼠海马神经元缺氧损伤具有明显的保护作用,其机制可能与减轻细胞内钙离子超载以及抗氧化损伤有关。
AIM: To investigate the protective effect and mechanism of oxysophoridine (OSR) on hypoxic injury of primary cultured neonatal rat hippocampal neurons. Methods: Primary cultured neonatal rat hippocampal neurons were used as experimental subjects. The hypoxic injury model was established by using glucose-free medium combined with physical hypoxia to determine the survival rate of neurons, the rate of lactate dehydrogenase (LDH) leakage and Changes of MDA, SOD, GSH-PX, NOS and NO in cells . The changes of intracellular free calcium concentration ([Ca2 +] i) in neurons were measured by fluorescence dual-wavelength spectrophotometer. Results: The hypoxia injury model group could cause neuron death in a short time, the rate of leakage of LDH increased, the content of MDA and NO increased, the activity of NOS increased, the activity of SOD and GSH-PX decreased and the intracellular [Ca2 +] i increased . OSR group (0.625,5,10μg.L-1) can reduce the damage of neurons to hypoxia model to varying degrees. CONCLUSION: Oxalipine base has a protective effect on hypoxic injury of hippocampal neurons in neonatal rats. The mechanism may be related to the reduction of intracellular calcium overload and anti-oxidative damage.