目的比较帕金森病(Parkinson disease,PD)患者和健康对照者多个脑结构的相位偏移值,探讨其诊断PD的价值。方法30例PD患者及30名年龄相匹配的健康对照者均在1.5 T MR系统中进行头部检查。采用磁敏感成像(susceptibility-weighted imaging...目的比较帕金森病(Parkinson disease,PD)患者和健康对照者多个脑结构的相位偏移值,探讨其诊断PD的价值。方法30例PD患者及30名年龄相匹配的健康对照者均在1.5 T MR系统中进行头部检查。采用磁敏感成像(susceptibility-weighted imaging,SWI)获得相位图,测量双侧尾状核、壳核、黑质致密带(substantianigra pars compacta,SNc)、黑质网状带(substantia nigra pars reticulata,SNr)、红核、脑脊液(cerebrospinal fluid,CSF)、额叶白质(frontal grey matter,FWM)及额叶皮质(frontal white matter,FGM)感兴趣区的相位偏移值。结果PD组SNc、尾状核、红核的相位偏移值均数较健康对照组明显降低(P<0.05),两组间SNr、壳核、CSF、FWM、FGM的相位偏移值差异无统计学意义(P>0.05)。结论通过测定PD患者脑感兴趣区相位偏移值可估测其脑内铁沉积。展开更多
Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mech...Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.展开更多
文摘目的比较帕金森病(Parkinson disease,PD)患者和健康对照者多个脑结构的相位偏移值,探讨其诊断PD的价值。方法30例PD患者及30名年龄相匹配的健康对照者均在1.5 T MR系统中进行头部检查。采用磁敏感成像(susceptibility-weighted imaging,SWI)获得相位图,测量双侧尾状核、壳核、黑质致密带(substantianigra pars compacta,SNc)、黑质网状带(substantia nigra pars reticulata,SNr)、红核、脑脊液(cerebrospinal fluid,CSF)、额叶白质(frontal grey matter,FWM)及额叶皮质(frontal white matter,FGM)感兴趣区的相位偏移值。结果PD组SNc、尾状核、红核的相位偏移值均数较健康对照组明显降低(P<0.05),两组间SNr、壳核、CSF、FWM、FGM的相位偏移值差异无统计学意义(P>0.05)。结论通过测定PD患者脑感兴趣区相位偏移值可估测其脑内铁沉积。
基金the National Natural Science Foundation of China (No. 30570627)
文摘Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.
