Jeon Songhee, Kim Youn Jung, Kim Seung-Tae, Moon Woongjoon, Chae Younbyoung, Kang Minjeong, Chung Mi-Young, Lee Hyangsook, Hong Mi-Sook, Chung Joo-Ho, Joh Tong H, Lee Hyejung, Park Hi-Joon
Medical Science Research Center, Dongguk University, Gyeonggi-Do, Republic of Korea.
Proteomics. 2008 Nov;8(22):4822-32. doi: 10.1002/pmic.200700955.
Acupuncture is frequently used as an alternative therapy for Parkinson's disease (PD), and it attenuates dopaminergic (DA) neurodegeneration in the substantia nigra (SN) in PD animal models. Using proteomic analysis, we investigated whether acupuncture alters protein expression in the SN to favor attenuation of neuronal degeneration. In C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg/day), intraperitoneal (i.p.) for 5 days, 2 or 100 Hz electroacupuncture (EA) was applied at the effective and specific acupoint, GB34, once a day for 12 consecutive days from the first MPTP treatment. Both treatments in MPTP mice led to restoration of behavioral impairment and rescued tyrosine hydroxylase (TH)-positive DA neurodegeneration. Using peptide fingerprinting MS, we identified changes in 22 proteins in the SN following MPTP treatment, and nine of these proteins were normalized by EA. They were involved in cell death regulation, inflammation, or restoration from damage. The levels of cyclophilin A (CypA), which is a neuroprotective agent, were unchanged by MPTP treatment but were increased in MPTP-EA mice. These results suggest that acupoint GB34-specific EA changes protein expression profiles in the SN in favor of DA neuronal survival in MPTP-treated mice, and that EA treatment may be an effective therapy for PD patients.
针灸常被用作帕金森病(PD)的替代疗法,并且在PD动物模型中可减轻黑质(SN)中的多巴胺能(DA)神经变性。我们使用蛋白质组学分析来研究针灸是否会改变SN中的蛋白质表达,以促进神经元变性的减轻。在用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP,30mg/kg/天)腹腔注射(i.p.)处理5天的C57BL/6小鼠中,从首次MPTP处理开始,每天一次在有效且特定的穴位GB34施加2或100Hz的电针(EA),连续12天。MPTP小鼠的这两种处理均导致行为障碍恢复,并挽救了酪氨酸羟化酶(TH)阳性的DA神经变性。使用肽指纹图谱质谱法,我们鉴定出MPTP处理后SN中22种蛋白质的变化,其中9种蛋白质经EA处理后恢复正常。它们参与细胞死亡调节、炎症或损伤修复。亲环素A(CypA)作为一种神经保护剂,其水平在MPTP处理后未发生变化,但在MPTP-EA小鼠中升高。这些结果表明,穴位GB34特异性EA可改变MPTP处理小鼠SN中的蛋白质表达谱,有利于DA神经元存活,并且EA治疗可能是PD患者的一种有效疗法。