Lee Yukyung, Choi Gaeun, Jeon Hyongjun, Kim Dongsoo, Ryu Sun, Koo Sungtae, Ha Ki-Tae, Kim Seungtae
Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Busandaehak-ro 49, Mulgeum-eup, Yangsan-si, Gyeongsangnam-do, 50612, Republic of Korea.
Korean Medicine Research Center for Healthy Aging, Pusan National University, Yangsan-si, Republic of Korea.
J Physiol Sci. 2018 Jul;68(4):455-462. doi: 10.1007/s12576-017-0547-7. Epub 2017 Jun 10.
Recent studies have suggested that increased oxidative stress is a potential etiology in Parkinson's disease (PD). In this study, we investigated whether acupuncture regulates antioxidants in the striatum (ST) of a PD mouse model. Male C57BL/6 mice were administered 30 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intraperitoneally once a day for 5 days and given acupuncture stimulation at SI3 or GB34 (Yanglingquan) was for 12 consecutive days. Dopaminergic neuronal survival in the nigrostriatal pathway and DJ-1 expression in the ST was evaluated by immunostaining, and the activities of superoxide dismutase (SOD) and catalase (CAT) in the ST was by enzyme-linked immunosorbent assay. MPTP administration induced dopaminergic neuronal death in the nigrostriatal pathway, which was suppressed by acupuncture stimulation at GB34. MPTP administration also suppressed DJ-1 expression and SOD and CAT activities in the ST, which were restored by acupuncture stimulation at GB34. These results indicate that the neuroprotective effect of acupuncture stimulation is due to regulation of the antioxidants.
最近的研究表明，氧化应激增加是帕金森病（PD）的一种潜在病因。在本研究中，我们调查了针刺是否能调节PD小鼠模型纹状体（ST）中的抗氧化剂。雄性C57BL/6小鼠每天腹腔注射30mg/kg的1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP），连续5天，并连续12天在SI3或GB34（阳陵泉）进行针刺刺激。通过免疫染色评估黑质纹状体通路中多巴胺能神经元的存活情况以及ST中DJ-1的表达，通过酶联免疫吸附测定法评估ST中超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性。MPTP给药导致黑质纹状体通路中多巴胺能神经元死亡，而GB34处的针刺刺激可抑制这种死亡。MPTP给药还抑制了ST中DJ-1的表达以及SOD和CAT的活性，而GB34处的针刺刺激可使其恢复。这些结果表明，针刺刺激的神经保护作用归因于对抗氧化剂的调节。
