Lu Juan, Liu Xuelei, Tian Ye, Li Hang, Ren Zhenxing, Liang Shuang, Zhang Guiyu, Zhao Caiping, Li Xinrong, Wang Tingting, Chen Dongfeng, Kuang Weihong, Zhu Meiling
Shenzhen Baoan Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Yuan 2 Road No. 25, Baoan District, Shenzhen 518133, China.
Quanzhou Medical College, Fujian 362100, China.
Evid Based Complement Alternat Med. 2019 Jul 31;2019:2735492. doi: 10.1155/2019/2735492. eCollection 2019.
The objective of this study was to explore the neuroprotective effect of moxibustion on rats with Parkinson's disease (PD) and its mechanism. A Parkinson's disease model was established in rats using a two-point stereotactic 6-hydroxydopamine injection in the right substantia nigra (SN) and ventral tegmental area. The rats received moxibustion at the Baihui (GV20) and Sishencong (EX-HN1) acupoints for 20 minutes, six times a week, for 6 weeks. The right SN tissue was histologically and immunohistochemically examined. Differentially expressed genes (DEGs) were identified through RNA sequencing. In addition, the levels of tyrosine hydroxylase (TH), glutathione peroxidase 4 (GPX4), and ferritin heavy chain 1 (FTH1) in SN were measured. In comparison to the model group, the moxibustion group showed a significantly greater TH immunoreactivity and a higher behavioural score. In particular, moxibustion led to an increase in the number and morphological stability of SN neural cells. The functional pathway analysis showed that DEGs are closely related to the ferroptosis pathway. GPX4 and FTH1 in the SN were significantly overexpressed in the moxibustion-treated rats with PD. Moxibustion can effectively reduce the death of SN neurons, decrease the occurrence of ferroptosis, and increase the TH activity to protect the neurons in rats with PD. The protective mechanism may be associated with suppression of the ferroptosis.
本研究的目的是探讨艾灸对帕金森病（PD）大鼠的神经保护作用及其机制。采用两点立体定向法将6-羟基多巴胺注射到大鼠右侧黑质（SN）和腹侧被盖区，建立帕金森病模型。大鼠在百会（GV20）和四神聪（EX-HN1）穴位接受艾灸20分钟，每周6次，共6周。对右侧SN组织进行组织学和免疫组织化学检查。通过RNA测序鉴定差异表达基因（DEG）。此外，检测SN中酪氨酸羟化酶（TH）、谷胱甘肽过氧化物酶4（GPX4）和铁蛋白重链1（FTH1）的水平。与模型组相比，艾灸组TH免疫反应性显著增强，行为评分更高。特别是，艾灸导致SN神经细胞数量增加和形态稳定性提高。功能通路分析表明，DEG与铁死亡通路密切相关。在接受艾灸治疗的PD大鼠中，SN中的GPX4和FTH1显著过表达。艾灸可有效减少SN神经元死亡，降低铁死亡的发生率，并增加TH活性，从而保护PD大鼠的神经元。其保护机制可能与抑制铁死亡有关。
