Lee Yukyoung, Lee Hanul, Bae Chang-Hwan, Seo Ji Eun, Kim Hee-Young, Koo Sungtae, Kim Seungtae
Department of Korean Medical Science, School of Korean Medicine, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongsangnam-do, 50612, Republic of Korea.
Korean Medicine Research Center for Healthy Aging, Pusan National University, 49 Busandaehak-ro, Mulgeum-eup, Yangsan-si, Gyeongsangnam-do, 50612, Republic of Korea.
J Tradit Complement Med. 2023 Jan 11;13(3):263-269. doi: 10.1016/j.jtcme.2023.01.005. eCollection 2023 May.
It has been reported that acupuncture at GB34 can enhance neurogenesis in the subventricular zone (SVZ) of mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). However, the signaling pathway that plays a critical role in neurogenesis needs to be established. Herein, we investigated the neurogenesis-promoting pathway mediated by acupuncture, focusing on extracellular signal-regulated kinase (ERK) signaling.
Male 10-week-old C57BL/6 mice were intraperitoneally injected with 30 mg/kg MPTP once daily for 5 days. Subsequently, mice were intraperitoneally injected with 50 mg/kg bromodeoxyuridine (BrdU), and electroacupuncture (EA) was performed at GB34 and BL60 for 3 weeks. The survival of dopaminergic neurons in the nigrostriatal pathway, cell proliferation in the SVZ, and expression levels of brain-derived neurotrophic factor (BDNF) and phosphorylated ERK (pERK) were evaluated.
MPTP induced dopaminergic neuronal death in the nigrostriatal pathway, and reduced the number of BrdU-positive and BrdU/doublecortin double-positive cells in the SVZ; these parameters were restored by EA. Moreover, EA prevented MPTP-induced reduction in striatal expression of BDNF and pERK. These results indicate that EA could prevent dopaminergic neuronal death in the nigrostriatal pathway and restore neurogenesis in the SVZ, which may be attributed to the activation of the BDNF-ERK pathway.
据报道,针刺足少阳胆经34穴(GB34)可增强1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理的小鼠脑室下区(SVZ)的神经发生。然而,在神经发生中起关键作用的信号通路仍有待确定。在此,我们研究了针刺介导的神经发生促进通路,重点关注细胞外信号调节激酶(ERK)信号通路。
10周龄雄性C57BL/6小鼠每天腹腔注射30mg/kg MPTP,连续注射5天。随后,小鼠腹腔注射50mg/kg溴脱氧尿苷(BrdU),并在GB34和膀胱经60穴(BL60)进行电针治疗3周。评估黑质纹状体通路中多巴胺能神经元的存活、SVZ中的细胞增殖以及脑源性神经营养因子(BDNF)和磷酸化ERK(pERK)的表达水平。
MPTP诱导黑质纹状体通路中多巴胺能神经元死亡,并减少SVZ中BrdU阳性和BrdU/双皮质素双阳性细胞的数量;电针恢复了这些参数。此外,电针可防止MPTP诱导的纹状体BDNF和pERK表达降低。这些结果表明,电针可防止黑质纹状体通路中多巴胺能神经元死亡,并恢复SVZ中的神经发生,这可能归因于BDNF-ERK通路的激活。