机构：[1]The Second Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China昆明医科大学附属第一医院神经外二科（微创神经外科）神经外科外科科室[2]Yunnan Provincial Clinical Research Center for Neurological Disease, Kunming 650032, Yunnan, China[3]Department of Neurology, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China内科科室神经内科昆明医科大学附属第一医院
Background: Parkinson's disease (PD) is a common central neurodegenerative disease in middle-aged and elderly people. The progressive degeneration and death of dopaminergic neurons leads to insufficient dopamine (DA) neurotransmitters. Acupuncture and moxibustion can alleviate the aging of neurons. Therefore, studying the neuroprotective effects of electroacupuncture (EA) in PD mice is particularly important. Methods: Intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 20 mg/kg) was used to establish a PD mouse model, and lipopolysaccharide (LPS) was used to induce microglia polarization. Western blotting, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), Nissl staining and immunohistochemistry were used to detect neuronal apoptosis and injury, alpha-syn expression and microglial accumulation in PD mice. In addition, the levels of inflammatory factors were determined using enzyme-linked immunosorbent assay (ELISA). Flow cytometry was used to detect the Ca2+ content. The fluorescein isothiocyanate (FITC) labeling method was used to assess glucose uptake. A reagent kit was used to detect glucose and lactate levels. Results: MPTP induced the selective loss of DA neurons in the SN of mice, altered Ca2+ homeostasis, and induced an inflammatory response. In addition, maintaining Ca2+ homeostasis depends on the activity of transient receptor potential channel 1 (TRPC1). EA therapy promotes TRPC1 expression, which has a negative regulatory effect on sodium-glucose cotransporter 1 (SGLT1). Under the action of EA, TRPC1 protein expression increased, Ca2+ concentrations increased, and the effect of SGLT1 was inhibited, thereby facilitating glucose metabolism, blocking the activation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway, restraining M1 polarization of microglia, and alleviating the PD process. Conclusion: EA promotes TRPC1/Ca2+ pathway activation, inhibits SGLT1-mediated regulation of glucose metabolism and PI3K/AKT pathway activation, inhibits microglial M1 polarization, and alleviates PD.
基金：
National Natural Science Foundation of China [82460236]; Training of Technological Innovation Talents in Yunnan Province [202205AD160006]; Associated Project of Yunnan Province Science & Technology Department and Kunming Medical University Basic Research for Application [202301AY070001-209]; Youth project of basic research project of Yunnan Science and Technology Plan Project [202401AU070011]; Yunnan Provincial Education Department Scientific Research Fund Project [2024J0183]; PhD Research Fund of the First Affiliated Hospital of Kunming Medical University [2022BS015]
第一作者机构：[1]The Second Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China[2]Yunnan Provincial Clinical Research Center for Neurological Disease, Kunming 650032, Yunnan, China
共同第一作者：
通讯作者：
通讯机构：[1]The Second Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, Yunnan, China[2]Yunnan Provincial Clinical Research Center for Neurological Disease, Kunming 650032, Yunnan, China
推荐引用方式(GB/T 7714)：
Zou Yanghong,Huang Tao,Pang Ailan,et al.Electroacupuncture regulates glucose metabolism by inhibiting SGLT1 levels, inhibiting microglial polarization, and alleviating Parkinson's disease[J].EXPERIMENTAL GERONTOLOGY.2024,196:doi:10.1016/j.exger.2024.112558.
