人参皂苷Rg1抗黑质神经元凋亡的可能机制
POSSIBLE MECHANISMS OF THE PROTECTIVE EFFECT OF GINSENOSIDE Rg1 ON APOPTOSIS IN SUBSTANTIA NIGRA NEURONS
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摘要: 目的研究人参皂苷Rg1抗1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)诱导的小鼠黑质神经元凋亡的作用及其机制。方法MPTP制备的帕金森病(Parkinson′s disease,PD)小鼠模型,经人参皂苷Rg1预处理后,用尼氏(Nissl)染色和TH组化染色观察黑质神经元的损害情况,借助TUNEL染色了解黑质神经元的凋亡情况,并用免疫组织化学方法检测黑质神经元caspase-3的活化以及iNOS和nNOS的表达情况。结果人参皂苷Rg1预处理能减少PD鼠模型黑质致密带Nissl阳性神经元和TH阳性神经元的脱失现象,降低黑质神经元TUNEL染色的阳性率。结论人参皂苷Rg1预处理对MPTP诱导的小鼠黑质神经元凋亡有明显的保护作用。Abstract: AIMTo investigate the role of ginsenoside Rg1 in preventing against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced apoptosis of the substantia nigra neurons in the mouse model of Parkinson′s disease (PD). METHODSC57Bl male mice were given MPTP ip in the PD model group. Different doses of ginsenoside Rg1 (2.5, 5.0 and 10.0 mg·kg-1) were given ip 3 days prior to MPTP in the pretreatment group. Nissl staining, tyrosine hydroxylase (TH) immunostaining and TdT-mediated dUTP nick-end labeling (TUNEL) staining were used to observe the damage of nigral neurons. The method of immunostaining was used to detect the caspase-3 activity, expression of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS). RESULTSPretreatment with ginsenoside Rg1 was shown to prevent the loss of Nissl staining neurons and TH-positive neurons, and decrease the percent of TUNEL-positive. Simultaneously, Rg1 was found to reduce caspase-3 activity and the expression of iNOS. CONCLUSIONGinsenoside Rg1 showed protective effect on MPTP-induced apoptosis in the mouse nigral neurons and this effect may be attributable to reducing the expression of iNOS and inhibiting the activation of caspase-3.
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