文献类型：期刊文献

英文题名：Research progress on neuroinflammatory mechanisms of acupuncture-moxibustion intervening Alzheimer disease

作者：Li, Li[1];Yan, Xingke[1];Ma, Cui[1];Wei, Yuting[1];Dou, Tingting[1];Xie, Wenting[1]

第一作者：李丽;李莉

通信作者：Yan, XK[1]

机构：[1]Gansu Univ Chinese Med, Sch Acupuncture & Tuina, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Acupuncture & Tuina, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;

年份：2026

卷号：24

期号：2

起止页码：190

外文期刊名：JOURNAL OF ACUPUNCTURE AND TUINA SCIENCE

收录：WOS:【ESCI(收录号:WOS:001748682200006)】；

基金：This study was supported by 2023 Key Talent Project of Gansu Province [2023, No. Gan Zu Tong Zi (2023)20 Hao]; 2024 University Teacher Innovation Fund Project (2024, No. 2024A-082); Research Startup Fund Project for Invited Talents of Gansu University of Chinese Medicine (No. 2024YJRC-06).

语种：英文

外文关键词：Acupuncture-moxibustion Therapy; Acupuncture Therapy; Moxibustion Therapy; Alzheimer Disease; Signal Transduction; Neuroinflammation

摘要：Relevant studies on acupuncture-moxibustion intervening Alzheimer disease (AD) were collected, sorted out, and summarized, and acupuncture-moxibustion plays its role in treating AD via the following aspects: inhibiting abnormal activation of microglia and astrocytes; correcting imbalanced polarization of microglia; upregulating the expression of triggering receptor expressed on myeloid cells 2 (TREM2) and component 1q (C1q); downregulating nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3); regulating the release of proinflammatory/anti-inflammatory factors; reducing the release of cyclooxygenase-2 (COX-2) and transforming growth factor-beta 1 (TGF-beta 1); suppressing the abnormal activation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3), nuclear factor-kappa B (NF-kappa B), high mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE), and p38 mitogen-activated protein kinase (p38 MAPK) pathways; and upregulating molecule levels of the interleukin (IL)-33/growth stimulating gene 2 protein (ST2) pathway.