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Electroacupuncture blocked motor dysfunction and gut barrier damage by modulating intestinal NLRP3 inflammasome in MPTP-induced Parkinson's disease mice.
Guo, Lei; Hu, Haiming; Jiang, Nan; Yang, Huabing; Sun, Xiongjie; Xia, Hui; Ma, Jun; Liu, Hongtao.
Afiliação
  • Guo L; College of Basic Medical Sciences, Hubei University of Chinese Medicine, Huangjiahu West Road 16, Wuhan 430065, China.
  • Hu H; College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan 430060, China.
  • Jiang N; School of Laboratory Medicine, Hubei University of Chinese Medicine, Huangjiahu West Road 16, Wuhan 430065, China.
  • Yang H; Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan 430061, China.
  • Sun X; Hubei Province Academy of Traditional Chinese Medicine, Wuhan, 430074, China.
  • Xia H; College of Basic Medical Sciences, Hubei University of Chinese Medicine, Huangjiahu West Road 16, Wuhan 430065, China.
  • Ma J; College of Basic Medical Sciences, Hubei University of Chinese Medicine, Huangjiahu West Road 16, Wuhan 430065, China.
  • Liu H; College of Basic Medical Sciences, Hubei University of Chinese Medicine, Huangjiahu West Road 16, Wuhan 430065, China.
Heliyon ; 10(9): e30819, 2024 May 15.
Article em En | MEDLINE | ID: mdl-38774094
ABSTRACT
Parkinson's disease (PD) is a neurodegenerative disorder commonly accompanied by gut dysfunction. EA has shown anti-inflammatory and neuroprotective effects. Here, we aim to explore whether EA can treat Parkinson's disease by restoring the intestinal barrier and modulating NLRP3 inflammasome. We applied 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to establish a PD mouse model and EA at the GV16, LR3, and ST36 for 12 consecutive days. The open-field test results indicated that EA alleviated depression and behavioral defects, upregulated the expressions of tyrosine hydroxylase (TH) and brain-derived neurotrophic factor (BDNF), and blocked the accumulation of α-synuclein (α-syn) in the midbrain. Moreover, EA blocked the damage to intestinal tissues of PD mice, indicative of suppressed NLRP3 inflammasome activation and increased gut barrier integrity. Notably, the antibiotic-treated mouse experiment validated that the gut microbiota was critical in alleviating PD dyskinesia and intestinal inflammation by EA. In conclusion, this study suggested that EA exhibited a protective effect against MPTP-induced PD by alleviating behavioral defects, reversing the block of motor dysfunction, and improving the gut barrier by modulating intestinal NLRP3 inflammasome. Above all, this study could provide novel insights into the pathogenesis and therapy of PD.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Heliyon Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China