文献类型：期刊文献

英文题名：Electroacupuncture promotes the repair of lacrimal glands damage in dry-eye animal models by modulating the BDNF/CREB signaling pathway

作者：Li, Liujiao[1,2];Shi, Li[1,2];Shen, Huxing[1];Liu, Xue[3];Luo, Dan[1,2];Ji, Huijie[1,2];Gao, Weiping[1,2];Wang, Jiaojiao[4]

第一作者：Li, Liujiao

通信作者：Gao, WP[1];Wang, JJ[2]

机构：[1]Nanjing Univ Chinese Med, Affiliated Hosp, Nanjing, Peoples R China;[2]Nanjing Univ Chinese Med, Nanjing, Peoples R China;[3]Gansu Univ Tradit Chinese Med, Affiliated Hosp, Dept Ophthalmol, Lanzhou, Peoples R China;[4]Henan Prov Peoples Hosp, Zhengzhou, Peoples R China

第一机构：Nanjing Univ Chinese Med, Affiliated Hosp, Nanjing, Peoples R China

通信机构：[1]corresponding author), Nanjing Univ Chinese Med, Affiliated Hosp, Nanjing, Peoples R China;[2]corresponding author), Henan Prov Peoples Hosp, Zhengzhou, Peoples R China.

年份：2026

卷号：16

期号：5

起止页码：480

外文期刊名：JOURNAL OF TRADITIONAL AND COMPLEMENTARY MEDICINE

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001859341300001)】；

基金：This project was supported by the National Natural Science Foundation of China (grant number: 82004426) .

语种：英文

外文关键词：Electroacupuncture; Dry eye disease; Lacrimal glands; BDNF/CREB signaling pathway

摘要：Background and aim: Dry eye disease (DED) is an eye disorder with global prevalence. Its treatment using electroacupuncture (EA) has shown exceptional clinical efficacy. This study aimed to examine the effectiveness of EA in treating DED and explore its underlying molecular mechanisms. Experimental procedure: A rabbit model of aqueous-deficient dry eye was established by subcutaneous injection of scopolamine hydrobromide. The EA and EA plus K252a (EA + K252a) groups underwent EA treatment (20 Hz, 0.5 ms, and 1 mA) for 15 min per session. The sham acupuncture (SA) group received blunt-tipped needling. These interventions were performed once daily for 14 days. At day 28 of the experiment, the role of the BDNF/ CREB pathway was examined by administration of the TrkB antagonist K252a. K252a was bilaterally injected into the lacrimal glands (LGs) in both the K252a and EA + K252a groups. Outcome measures included tear film break-up time (BUT), corneal fluorescein staining (FL), Schirmer I tear test (SIT), and pathological changes in the ocular surface and LGs. The levels of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), phospho-phosphatidylinositol 3-kinase (p-PI3K), phospho-protein kinase B (p-AKT), cyclic adenosine monophosphate response element-binding protein (CREB), and phospho-cyclic adenosine monophosphate response element-binding protein (p-CREB) were assessed. Results and conclusion: Experimental results showed that EA facilitates the restoration of damaged LGs, extends BUT, decreases FL, and enhances SIT by regulating the proteins involved in the BDNF/CREB pathway. Consequently, these improvements effectively alleviate the symptoms associated with DED.