β-Endorphin Mediates ElectronicAcupunccuration-Institutioned Remieliation с помощью модуляции линии нейронных стволовых клеток в экспериментальном аутоиммунном энцефаломиэлите.
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Wang Yanping, Ma Xiaoru, Qiao Zhixin, Zhuang Wei, Zhang Xiyu, Luo Jingyu, Wu Junfeng, Li Anqi, Wang Chao, Ji Jiayu, Xiu Xin, Wang Jing, Meng Yanting, Huang Wei, Zhang Sifan, Lang Xiujuan, Liu Xijun, Sun Bo, Li Hulun, Liu Yumei
Аннотация
Оригинал публикации
β-Endorphin Mediates Electroacupuncture-Induced Remyelination via Neural Stem Cell Lineage Modulation in Experimental Autoimmune Encephalomyelitis.
AIMS: Effective remyelination in multiple sclerosis (MS) requires both the proliferation of endogenous neural stem cells (NSCs) and their lineage-specific differentiation into oligodendrocyte progenitor cells (OPCs). This study aimed to investigate whether electroacupuncture (EA) promoted NSC proliferation and OPC differentiation via β-endorphin (β-EP)-mediated opioid signaling in a murine model of MS.
METHODS: Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice to model MS. EA stimulation was applied daily at the Zusanli (ST36) acupoint. NSC proliferation and OPC differentiation were assessed via immunofluorescence, flow cytometry (FCM), and RT-qPCR. β-EP expression and opioid receptor involvement were evaluated in the hypothalamus and subventricular zone (SVZ). Naloxone, a nonselective opioid receptor antagonist, was used to determine the role of opioid signaling in EA-induced effects.
RESULTS: EA significantly enhanced NSC proliferation and increased the proportion of NSC-derived OPCs in the SVZ of EAE mice. EA treatment improved clinical score, reduced demyelination, and attenuated leukocyte infiltration of the central nervous system (CNS). Mechanistically, EA upregulated β-EP and its precursor pro-opiomelanocortin (POMC), along with opioid receptors μ-opioid receptor (MOR) and κ-opioid receptor (KOR) (encoded by Oprm1 and Oprk1, respectively). Naloxone administration abolished the beneficial effects of EA on NSC behavior and remyelination, confirming the involvement of opioid receptor-dependent β-EP signaling.
CONCLUSION: EA promotes remyelination in EAE mice by stimulating β-EP-mediated NSC proliferation and OPC differentiation. These findings reveal a novel neuroregenerative mechanism and support EA as a promising adjunctive strategy for demyelinating diseases such as MS.