ArticleJournal of immunology research2026
Electroacupuncture Ameliorates Scopolamine-Induced Dry Eye Disease in Mice by Restoring Lacrimal Gland Lipid Homeostasis and Reducing IL-1β/IL-18 Expression.
Article in Journal of immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Electroacupuncture Ameliorates Scopolamine-Induced Dry Eye Disease in Mice by Restoring Lacrimal Gland Lipid Homeostasis and Reducing IL-1β/IL-18 Expression.Journal of immunology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Dry eye disease (DED) can lead to severe eye discomfort, which manifests as dryness, pain and decreased vision, and significantly affects daily life. This study elucidated the effects of electroacupuncture (EA) intervention on DED and clarified its potential mechanisms through changes in lacrimal gland lipid metabolism and inflammation. A DED mouse model was established by repeated subcutaneous injections of scopolamine hydrobromide, followed by EA intervention. The therapeutic effects of EA intervention on DED were determined based on tear secretion volume (n = 10), corneal fluorescein staining scores (n = 10), corneal stromal (CS) damage (n = 6), and changes in corneal and lacrimal gland morphology (n = 10). Mechanistic endpoints included lacrimal gland lipidomic profiling by ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) (n = 6) and assessment of IL-1β and IL-18 expression by immunohistochemistry (n = 6), western blotting (n = 3) and qRT-PCR (n = 6). EA increased tear secretion, reduced corneal fluorescein staining and ameliorated CS and lacrimal gland pathological alterations. Lipidomic analysis identified 81 metabolites, and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analysis highlighted arachidonic acid metabolism and inflammation-related pathways. EA reduced arachidonic acid and several downstream pro-inflammatory metabolites while partially restoring omega-3 polyunsaturated fatty acids (PUFAs) and their derivatives. EA also reduced lacrimal gland IL-1β and IL-18 expression at the protein and mRNA levels. These findings suggest that EA may ameliorate scopolamine-induced DED, at least in part, through modulation of lacrimal gland lipid homeostasis and suppression of inflammatory responses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.