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Updated: Jun 4, 2025

Establishment of A Mouse Model of Aqueous Deficiency Dry Eye
Published on: November 1, 2024
Caffeine's protective role in dry eye disease and meibomian gland dysfunction: insights from clinical and
Yu-Zhi Li1, Chao Wang1, Xi Peng1
1Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Purpose:
Inflammation and apoptosis contribute to the development of dry eye disease (DED) and meibomian gland dysfunction (MGD). This study aimed to investigate the effect of caffeine on the ocular surface and tear inflammatory cytokines through clinical, in vivo, and in vitro experiments.
Methods:
In the clinical study, comprehensive ophthalmic examinations of participants in the control and the caffeine groups were compared, including ocular surface and tears inflammatory cytokines. For in vitro study, rat meibomian gland epithelial cells (RMGECs) and human corneal epithelial cells (HCECs) were pretreated with or without caffeine and then stimulated with lipopolysaccharide (LPS). Inflammatory responses, apoptosis, and differentiation in cells were analyzed. In vivo study, apolipoprotein E knockout (ApoE-/-) mice were given caffeine-diet or no caffeine-diet, and their meibomian glands (MGs) and corneal tissue were compared.
Results:
Participants in the caffeine group exhibited significantly healthier ocular surface, lower tears inflammatory cytokines and a reduced prevalence of DED compared to the control group. In vitro study, caffeine pretreatment attenuated inflammatory responses, apoptosis and differentiation in LPS-induced RMGECs. Meanwhile, caffeine also markedly suppressed inflammatory responses and apoptosis in LPS-induced HCECs. In vivo study showed that ApoE-/- mice with caffeine-diet had more normal morphology of MGs and corneas compared to those without caffeine-diet, along with reduced inflammatory responses, cells apoptosis and ductal keratinization. Both in vitro and in vivo studies indicated that caffeine treatment was observed to inactivate of nuclear factor kappa B (NF-κB) phosphorylation.
Conclusions:
Our study indicated that caffeine may be a protective potential of ocular surface, providing a new perspective on clinical treatment for DED and MGD.
Insights
Caffeine intake may protect the ocular surface by reducing inflammation and apoptosis, offering a potential new treatment for dry eye disease (DED) and meibomian gland dysfunction (MGD).
Area of Science:
- Ophthalmology
- Cell Biology
- Immunology
Background:
- Dry eye disease (DED) and meibomian gland dysfunction (MGD) are linked to ocular surface inflammation and cell death.
- Current treatments for DED and MGD have limitations.
Purpose of the Study:
- To investigate the therapeutic potential of caffeine on the ocular surface.
- To examine caffeine's effects on tear inflammatory cytokines, inflammation, and apoptosis in DED and MGD models.
Main Methods:
- Clinical study comparing participants receiving caffeine versus a control.
- In vitro experiments using rat meibomian gland epithelial cells (RMGECs) and human corneal epithelial cells (HCECs) treated with caffeine and lipopolysaccharide (LPS).
- In vivo study using apolipoprotein E knockout (ApoE-/-) mice fed a caffeine-containing diet.
Main Results:
- Caffeine consumption led to a healthier ocular surface, reduced tear inflammatory cytokines, and lower DED prevalence in clinical participants.
- In vitro studies showed caffeine attenuated inflammation and apoptosis in LPS-stimulated RMGECs and HCECs.
- In vivo studies demonstrated improved meibomian gland and corneal morphology, with reduced inflammation and apoptosis in caffeine-fed mice. Caffeine inactivated nuclear factor kappa B (NF-κB) phosphorylation.
Conclusions:
- Caffeine exhibits protective effects on the ocular surface.
- Caffeine presents a novel therapeutic avenue for managing DED and MGD.
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