Polygalae radix inhibits toxin-induced neuronal death in the Parkinson's disease models

被引:67
作者
Choi, Jin Gyu [1 ,2 ]
Kim, Hyo Geun [1 ,2 ]
Kim, Min Cheol [3 ]
Yang, Woong Mo [4 ]
Huh, Youngbuhm [5 ]
Kim, Sun Yeou [3 ]
Oh, Myung Sook [1 ,2 ]
机构
[1] Kyung Hee Univ, Dept Oriental Pharmaceut Sci, Coll Pharm, Seoul 130701, South Korea
[2] Kyung Hee Univ, Kyung Hee EW Pharmaceut Res Inst, Seoul 130701, South Korea
[3] Kyung Hee Univ, Grad Sch EW Med Sci, Yongin 449701, South Korea
[4] Kyung Hee Univ, Dept Prescriptionol, Coll Oriental Med, Seoul 130701, South Korea
[5] Kyung Hee Univ, Coll Med, Dept Anat & Neurobiol, Seoul 130701, South Korea
关键词
Polygalae radix; Parkinson's disease; Dopaminergic neuron; OXIDATIVE STRESS; NITRIC-OXIDE; PC12; CELLS; SUBSTANTIA-NIGRA; TENUIFOLIA ROOT; MECHANISMS; SUPEROXIDE; CASPASE-3; DAMAGE; RAT;
D O I
10.1016/j.jep.2010.12.030
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Aim of the study: Polygalae radix, the root of Polygala tenuifolia Willd, has commonly been used for the treatment of amnesia and anxiety in traditional Korean medicine. The aim of this study was to investigate its neuroprotective effects and possible mechanisms of action in models of Parkinson's disease. Materials and methods: This study utilized a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, a reactive oxygen species (ROS) assay, a nitric oxide (NO) production assay, and a caspase-3 activity test as measures of cell viability in PC12 cells damaged by 6-hydroxydopamine (6-OHDA). The protective effects of PRE against 1-methyl-4-phenylpyridium (MPP+)-induced neurotoxicity were assessed in rat primary dopaminergic neurons and in a mouse PD model in which PRE was administered (100 mg/kg/day, 3 days, p.o.) before acute 1-mehtyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. Finally, TH immunohistochemistry tests were conducted in the substantia nigra pars compacta (SNpc) and striatum (ST). Results and conclusions: PRE significantly inhibited 6-OHDA-induced cell damage at doses of 0.05-1 mu g/ml with a maximal effect at 0.1 mu g/ml. Caspase-3 activity and the production of ROS and NO were alleviated at 0.1 mu g/ml. Also at this dose, PRE protected mesencephalic dopaminergic neurons from MPP+-induced toxicity. In an in vivo mouse model of PD, PRE protected dopaminergic neurons and fibers from MPTP-induced toxicity in the SNpc and ST. These results demonstrate that PRE has protective effects on dopaminergic neurons via its anti-oxidant and anti-apoptotic activity. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:414 / 421
页数:8
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