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韩国红参对帕金森病小鼠模型纹状体影响的蛋白质组学分析

Proteomic Analysis of the Effect of Korean Red Ginseng in the Striatum of a Parkinson's Disease Mouse Model.

作者信息

Kim Dongsoo, Jeon Hyongjun, Ryu Sun, Koo Sungtae, Ha Ki-Tae, Kim Seungtae

机构信息

Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Republic of Korea.

出版信息

PLoS One. 2016 Oct 27;11(10):e0164906. doi: 10.1371/journal.pone.0164906. eCollection 2016.

DOI:10.1371/journal.pone.0164906
PMID:27788166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5082921/
Abstract

Recent studies have shown that Korean Red Ginseng (KRG) suppresses dopaminergic neuronal death in the brain of a Parkinson's disease (PD) mouse model, but the mechanism is still elusive. Using a 2-dimensional electrophoresis technique, we investigated whether KRG can restore the changes in protein expressions in the striatum (ST) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-injected mice. Male C57BL/6 mice (9 weeks old) were injected with 20 mg/kg MPTP intraperitoneally four times at 2-h intervals. KRG (100 mg/kg) was orally administered once a day for 3 days from one hour after the first MPTP injection. Two hours after the third KRG administration a pole test was performed to evaluate motor function, after which the brains were immediately harvested. Survival of dopaminergic neurons in the nigrostriatal pathway and protein expression in the ST were measured by immunohistochemistry and 2-dimensional electrophoresis. KRG suppressed MPTP-induced behavioral dysfunction and neuronal death in the nigrostriatal pathway. Moreover, 30 proteins changed by MPTP and KRG in the ST were identified and shown to be related to glycolysis/gluconeogenesis and neurodegenerative diseases including Alzheimer's disease and PD. KRG has neuroprotective effects against MPTP toxicity and alleviates protein expression profiles related to enhancing energy metabolism in the ST of MPTP-treated mice.

摘要

最近的研究表明,韩国红参(KRG)可抑制帕金森病(PD)小鼠模型脑中多巴胺能神经元的死亡,但其机制仍不清楚。我们使用二维电泳技术,研究了KRG是否能恢复1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)注射小鼠纹状体(ST)中蛋白质表达的变化。雄性C57BL/6小鼠(9周龄)每隔2小时腹腔注射20mg/kg MPTP,共注射4次。从首次注射MPTP后1小时起,每天口服一次KRG(100mg/kg),持续3天。在第三次给予KRG后2小时进行爬杆试验以评估运动功能,之后立即摘取大脑。通过免疫组织化学和二维电泳检测黑质纹状体通路中多巴胺能神经元的存活情况以及ST中的蛋白质表达。KRG可抑制MPTP诱导的行为功能障碍和黑质纹状体通路中的神经元死亡。此外,还鉴定出ST中30种因MPTP和KRG而发生变化的蛋白质,这些蛋白质与糖酵解/糖异生以及包括阿尔茨海默病和PD在内的神经退行性疾病有关。KRG对MPTP毒性具有神经保护作用,并可缓解与MPTP处理小鼠ST中能量代谢增强相关的蛋白质表达谱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/6a230b8fbcbb/pone.0164906.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/4aff6fa46127/pone.0164906.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/3c3a6fa4450f/pone.0164906.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/b7261b2e92fa/pone.0164906.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/79e2d3e183b8/pone.0164906.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/ba8fca281747/pone.0164906.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/6a230b8fbcbb/pone.0164906.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/4aff6fa46127/pone.0164906.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/3c3a6fa4450f/pone.0164906.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/b7261b2e92fa/pone.0164906.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/79e2d3e183b8/pone.0164906.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/ba8fca281747/pone.0164906.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4a9/5082921/6a230b8fbcbb/pone.0164906.g006.jpg

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