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作 者:赵靖[1] 吴洋[1] 孙苗[2] 王洁[3] 李云鸿[4] 张快[1] 余建强[1,5]
机构地区:[1]宁夏医科大学药理学系,宁夏银川750004 [2]宁夏医科大学生育力保持重点实验室,宁夏银川750004 [3]宁夏医学科学研究所,宁夏银川750004 [4]宁夏医科大学科学技术中心,宁夏银川750004 [5]宁夏回药现代化工程研究中心,宁夏银川750004
出 处:《中国中药杂志》2012年第1期94-98,共5页China Journal of Chinese Materia Medica
基 金:国家自然科学基金项目(309605060);宁夏自然科学基金项目(NZ11212);银川市科技公关项目(银财字[2009]309);宁夏医科大学重点项目(XZ200803)
摘 要: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。Objective: To investigate the protective effects of oxysophoridine(OSR) on primary cultured hippocampus neurons subjected to anoxia injury in neonatal rats and its mechanism.Method: The model of anoxia injury of hippocampus neurons in neonatal rats were primarily cultured in vitro by physical oxygen deficiency using glucose-free culture fluid.The survival rate of neurons,the leaking rate of lactate dehydrogenase(LDH),the intracellular contents of malondialdehyde(MDA) and nitric oxide(NO),the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-PX) and nitric oxide synthase(NOS) were measured.The intracellular free calcium concentration(i) in hippocampus neurons were detected with Ca2+-sensitive dual wavelength fluorescence spectrophotometer.Result: Neuron death occurred in the anoxia injury model group with increase of LDH leaking rate,the contents of NO,MDA,intracellular i and the elevated activity of NOS while decreased activities of SOD and GSH-PX.The hippocampus neurons subjected to anoxia injury were alleviated in OSR(0.625,5,10 μg·L-1) group.Conclusion: OSR has significant protective effects on hippocampus neurons subjected to anoxic injury.The mechanism of its protective effect may relate to its reduction of calcium overload and against oxidation injury.
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