Kim Dongsoo, Kwon Sunoh, Jeon Hyongjun, Ryu Sun, Ha Ki-Tae, Kim Seungtae
Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Republic of Korea.
KM Fundamental Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
J Ginseng Res. 2018 Oct;42(4):429-435. doi: 10.1016/j.jgr.2017.04.008. Epub 2017 Apr 28.
Recent studies have shown that Korean Red Ginseng (KRG) successfully protects against dopaminergic neuronal death in the nigrostriatal pathway of a Parkinson's disease (PD) mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration; however, the mechanism has yet to be identified. Therefore, in this study we used two-dimensional electrophoresis to investigate the effects of KRG on the changes in protein expression in the substantia nigra (SN) of MPTP-treated mice.
Male C57BL/6 mice (9 wk old) were intraperitoneally administered MPTP (20 mg/kg) four times at 2-h intervals, after which KRG (100 mg/kg) was orally administered once a day for 5 d. Two hours after the fifth KRG administration, a pole test was conducted to evaluate motor function, after which the brains were immediately collected. Survival of dopaminergic neurons was measured by immunohistochemistry, and protein expression was measured by two-dimensional electrophoresis and Western blotting.
KRG alleviated MPTP-induced behavioral dysfunction and neuronal toxicity in the SN. Additionally, the expression of eight proteins related to neuronal formation and energy metabolism for survival were shown to have changed significantly in response to MPTP treatment or KRG administration. KRG alleviated the downregulated protein expression following MPTP administration, indicating that it may enhance neuronal development and survival in the SN of MPTP-treated mice.
These findings indicate that KRG may have therapeutic potential for the treatment of patients with PD.
最近的研究表明，韩国红参（KRG）成功地保护了由1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的帕金森病（PD）小鼠模型黑质纹状体通路中的多巴胺能神经元死亡；然而，其机制尚未确定。因此，在本研究中，我们使用二维电泳来研究KRG对MPTP处理小鼠黑质（SN）中蛋白质表达变化的影响。
雄性C57BL/6小鼠（9周龄）每隔2小时腹腔注射MPTP（20mg/kg）4次，之后每天口服KRG（100mg/kg），持续5天。在第五次给予KRG后2小时，进行爬杆试验以评估运动功能，之后立即收集大脑。通过免疫组织化学测量多巴胺能神经元的存活情况，并通过二维电泳和蛋白质印迹法测量蛋白质表达。
KRG减轻了MPTP诱导的行为功能障碍和SN中的神经元毒性。此外，显示与神经元形成和存活的能量代谢相关的8种蛋白质的表达在MPTP处理或KRG给药后发生了显著变化。KRG减轻了MPTP给药后蛋白质表达的下调，表明它可能增强MPTP处理小鼠SN中的神经元发育和存活。
这些发现表明KRG可能对PD患者具有治疗潜力。
