摘要
目的 :研究人参皂苷Rg1对 1 甲基 4 苯基 1 ,2 ,3 ,6 四氢吡啶 (1 methyl 4 phenyl 1 ,2 ,3 ,6 tetra hydropyridine,MPTP)诱导的小鼠黑质神经元凋亡的抗氧化保护作用。方法 :采用MPTP制备帕金森病(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存活情况 ,通过活化型Caspase 3的免疫组化染色和TUNEL染色了解黑质神经元的凋亡情况 ,并用生化技术对黑质区域谷胱甘肽 (GSH)浓度及超氧化物歧化酶 (SOD)活力进行检测。结果 :人参皂苷Rg1预处理能提高黑质区域GSH的浓度及降低SOD活力 ,相应地减少PD鼠黑质致密带Nissl阳性神经元和TH阳性神经元的脱失现象 ,使活化型Caspase 3表达阳性细胞减少 ,降低黑质神经元TUNEL染色的阳性率。结论
AIM: To explore the role of ginsenoside Rg1 as an antioxidan t in preventing against 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) -induced apoptosis of substantia nigra neurons in Parkinson's disease (PD) mice models. METHODS: C57BL mice were administrated (sc) with MPTP t o produce PD mice models. Different doses ( 5.0 , 10.0 , and 20.0 mg·k g -1 ) of Rg1 were given (ip) MPTP prior 3 days in the pretreatment groups. Nissl staining, tyrosinehydroxythase (TH) immunostaining, cleaved caspase 3 immu nostaining, and TUNEL staining were used to observe the changes of nigra neurons . Meanwhile, biochemical technique was used to detect the concentration of GSH a nd the vitality of SOD in substantia nigra. RESULTS: Pretreatmen t with Rg1 could increase the concentration of GSH and descent the vitality of S OD in substantia nigra, prevent the loss of Nissl staining neurons and TH-posit ive neurons, and decrease the percent of cleaved caspase 3 and TUNEL-positive c ells. CONCLUSION: Down-regulation of oxidative stress is the po ssible mechanism of ginsenoside Rg1 protecting the substantia nigra neurons in P D mice.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2003年第3期273-277,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
福建省科技厅和教育厅科学研究项目基金资助课题 (№ :2 0 0 1Z0 37JA0 2 2 19)
