Model Introduction
Dry Eye Disease (DED) is a chronic disease caused by abnormalities in tear quality, quantity, or dynamics, leading to tear film instability and imbalance of the ocular surface microenvironment. It is often accompanied by ocular surface inflammatory responses (conjunctival inflammatory damage), tissue damage, and neurosensory abnormalities.
To simulate human ocular surface lesions caused by different etiologies, we provide various animal models that highly replicate clinical pathological features, covering induction methods such as chemical damage, environmental stimulation, and metabolic disorders. These aim to provide a reliable experimental platform for the development of novel ophthalmic drugs (e.g., artificial tears, anti-inflammatory drugs, targeted therapies).
Core Model Classifications:
- Preservative-Induced Model (BAC Model): Induced by Benzalkonium Chloride (BAC), simulating ocular surface toxicity and inflammation from long-term eye drop use.
- Environmental Stress Model (Mixed Type): Low-humidity environment combined with cholinergic receptor antagonists (Scopolamine), simulating dry eye symptoms in modern arid environments.
- Lifestyle-Related Model: Includes sleep deprivation and blue light irradiation models, studying the damage of modern light pollution and abnormal sleep patterns on the ocular surface.
- Metabolic Disorder-Related Model: Includes High-Fat Diet (HFD) and Diabetes Mellitus (DM) induced models, focusing on Meibomian/lacrimal gland dysfunction.
Research Applications
This series of models is widely applied in:
- Efficacy Evaluation: Assessing the effects of anti-inflammatory drugs, immunosuppressants, secretagogues, and ocular surface repair agents.
- Pathogenesis Exploration: Studying ocular surface epithelial apoptosis, conjunctival goblet cell loss, squamous metaplasia, and changes in the ocular surface immune microenvironment.
- Barrier Function Research: Investigating the impact of tear film instability on the corneal and conjunctival barriers.
- Ocular Complications of Systemic Diseases: Exploring the damage mechanisms of metabolic diseases like hyperlipidemia and diabetes on the Meibomian and lacrimal glands.
Key Points of Experimental Design
We strictly control modeling parameters to ensure high consistency:
- Chemical Induction: Precise control of BAC concentration and frequency to observe chronic damage to corneal epithelium and conjunctival tissue.
- Environmental Intervention: Establishing a constant low-humidity dehumidification device combined with scopolamine to inhibit parasympathetic nerves, significantly reducing tear secretion.
- Stress Simulation: Using standardized sleep deprivation devices or specific wavelength LED blue light to simulate physical/neural stress in modern life.
- Metabolic Induction: Long-term high-fat diet or Streptozotocin (STZ) induction of diabetes, focusing on lacrimal gland lipid deposition and inflammatory activation.
Key Monitoring Indicators
We provide comprehensive ocular surface assessment technical support: 1. Clinical Sign Observation
- Slit-lamp Examination: Observing eyelid and conjunctival hyperemia and corneal transparency.
- Corneal Fluorescein Sodium Staining (FL): Evaluating corneal epithelial damage and repair.
- Schirmer Test: Quantitatively assessing lacrimal gland secretory function. 2. Histopathological Analysis
- HE Staining: Observing morphological changes in lacrimal glands, Meibomian glands, and conjunctival tissues (e.g., inflammatory cell infiltration, glandular atrophy).
- PAS Staining: Precise counting of conjunctival goblet cells to evaluate ocular surface lubrication.
- IHC/IF: Detecting inflammatory cytokines (e.g., CD4+, Ly6g, F4/80) and structural proteins (e.g., Collagen IV). 3. Biochemical and Molecular Indicators
- Tear Break-up Time (BUT): Evaluating tear film stability.
- Oxidative Stress Indicators: Monitoring lipid peroxidation levels in the lacrimal gland.
- Blood Glucose/Lipid Monitoring: Ensuring successful modeling for metabolic-type models.
