节点文献

褪黑素通过抑制线粒体通透性转换孔开放保护缺氧缺糖SHSY 5Y细胞

Melatonin protects SHSY5Y neuronal cells from oxygen-glucose deprivation by inhibiting the opening of the mitochondrial permeability transition pore

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 邹良玉褚晓凡

【Author】 ZOU Liang-yu,CHU Xiaofan.(Departments of Neurology,Second clinical College University of Jinan,Shenzhen 518020,China)

【机构】 暨南大学医学院附属二院神经内科暨南大学医学院附属二院神经内科 广东深圳518020广东深圳518020

【摘要】 目的观察褪黑素对体外缺氧缺糖SHSY 5Y细胞的保护作用及线粒体通透性转换孔开放对该保护作用的影响。方法体外培养SHSY 5Y神经母细胞瘤株,以缺氧缺糖(OGD)、褪黑素(10μm o l/L)伴或不伴苍术苷(atracty los ide)(20μm o l/L)处理,以M TT检测SHSY 5Y细胞活性,应用ca lce in-AM、HE t和fluo-3/AM的荧光强度测定OGD后SHSY 5Y细胞线粒体通透性转换孔(M TPT)开放、细胞内超氧阴离子和钙离子的浓度。结果褪黑素能提高OGD后SHSY 5Y细胞的活性,这种神经保护作用可被苍术苷阻断。褪黑素降低OGD后ca lce in-AM、HE t和fluo-3/AM的荧光强度。结论褪黑素通过抑制SHSY 5Y细胞M TPT开放,来降低细胞内超氧阴离子的浓度,进而抑制细胞内钙超载,从而达到保护SHSY 5Y细胞对抗OGD的细胞损害的作用。

【Abstract】 Objective To investigate the neuroprotective effect of melatonin on SHSY5Y neuronal cells against oxygen-glucose deprivation(OGD),and the role of the opening of the mitochondrial permeability transition pore(MPTP)in the effect.Methods SHSY5Y neuroblastoma cells were exposed to OGD,melatonin(10μM)alone or melatonin together with atractyloside(20 μmol/L).Cell viability was measured by the MTT assay,opening of MPTP,intracellular concentration of superoxide anion and calcium were evaluated via the fluorescence intensity of calcein-AM,HEt and fluo-3/AM.Results After OGD,compared with the vehicle group,the MTT value was elevated significantly in the melatonin group(P<(0.01)).The neuroprotective effect of melatonin was blocked by administration of atractyloside.The fluorescence intensity of calcein-AM(P<(0.05)),HEt(P<(0.05))and fluo-3/AM(P<(0.01))was decreased significantly in the melatonin group.Conclusion Melatonin protects SHSY5Y neuronal cells against OGD by inhibiting the opening of MPTP and reducing the intracellular concentration of superoxide anion and calcium.

  • 【文献出处】 中风与神经疾病杂志 ,Journal of Apoplexy and Nervous Diseases , 编辑部邮箱 ,2006年03期
  • 【分类号】Q576
  • 【下载频次】171
节点文献中: 

本文链接的文献网络图示:

本文的引文网络