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作 者:樊丽[1] 李世玲[2] 伊超[3] 周丽[1] 岳丽玲[1] 许惠玉[4]
机构地区:[1]齐齐哈尔医学院医药科学研究院,齐齐哈尔161006 [2]齐齐哈尔医学院附属第一医院药局,齐齐哈尔161041 [3]齐齐哈尔医学院附属第二医院神经外科,齐齐哈尔161006 [4]齐齐哈尔医学院医学技术学院,齐齐哈尔161006
出 处:《医药导报》2017年第5期473-476,共4页Herald of Medicine
基 金:黑龙江省教育厅科学技术研究项目(12531809)
摘 要:目的探讨低分子姬松茸多糖(LMPAB)对过氧化氢(H_2O_2)诱导大鼠海马神经细胞氧化损伤的影响及其可能机制。方法新生SD大鼠海马神经细胞分离培养,分为正常对照组(加入等量的培养液)、模型对照组(加入500μmol·L^(-1)H_2O_2)和LMPAB大、中、小剂量组(分别加入20,10,5 mg·L^(-1)LMPAB预处理后,加入500μmol·L^(-1)H_2O_2)。采用噻唑蓝(MTT)法测定海马神经细胞活性;流式细胞仪检测海马神经细胞线粒体膜电位(MMP);按照试剂说明书介绍的方法检测丙二醛(MDA)含量及过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)活性。结果正常对照组和LMPAB大剂量组的细胞活性、CAT活性、SOD活性、GSH-PX活性及MMP均显著高于模型对照组(均P<0.01);MDA含量均明显低于模型对照组(均P<0.01)。结论 LMPAB对H_2O_2诱导的大鼠海马神经细胞氧化损伤有一定的拮抗作用,机制可能与LMPAB增强海马神经细胞抗氧化能力有关。Objective To investigate the effect and the potential mechanisms of low molecular polysaccharide from agaricus blazei (LMPAB) on H2O2-induced oxidative injury in hippocampal neuronal cells of rats.Methods Hippocampal neuronal cells were isolated from SD rats (24 h) and grew in culture.Cultured cells were divided into normal control group (added the same amount of nutrient solution), model control group (added 500 μmol·L-1H2O2 solution) and LMPAB high, medium, low dose groups (added 20,10,5 mg·L-1 LMPAB solution, respectively, then added 500 μmol·L-1 H2O2 solution each).The hippocampal neuron cell activity was detected with MTT method.The hippocampus neuron mitochondrial membrane potential (MMP) was detected by flow cytometry.According to the reagent instruction methods, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities were detected.Results The activities of cell, CAT, SOD, GSH-PX and MMP in normal control group and the LMPAB high dose group were significantly higher than those of model control group (P〈0.01);The content of MDA in normal control group and LMPAB high dose group was significantly lower than that of model control group (P〈0.01).Conclusion The protective effect of LMPAB on hippocampal neurons with H2O2-induced injury may be related with the mechanism of enhancing the neuronal antioxidative capacity.
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