Model Introduction
Corneal injury is not limited to physical trauma; modern medical research focuses more on chronic ocular surface damage caused by environmental factors, chemicals, metabolic diseases, and lifestyles. MDL provides various animal models of human corneal injury and Dry Eye Disease (DED) that highly simulate clinical pathological features. These models can replicate pathological processes such as tear film instability, corneal epithelial cell apoptosis, goblet cell loss, and ocular surface inflammation, serving as ideal alternatives for studying corneal repair, ophthalmic drug screening, and pathogenesis.
Research Applications
- Drug R&D and Screening: Evaluating the efficacy of artificial tears, anti-inflammatory drugs (e.g., Cyclosporine), and novel targeted drugs on corneal epithelial repair.
- Pathogenesis Exploration: Studying the effects of oxidative stress, inflammatory cytokines, abnormal innervation, and metabolic disorders on corneal health.
- Clinical Translational Research: Simulating damage caused by modern lifestyle factors (blue light, sleep deprivation, high-fat diet) to provide a basis for clinical prevention.
- Medical Device Evaluation: Assessing the biocompatibility of contact lens care solutions and ophthalmic surgical consumables with the cornea.
Key Points of Experimental Design
To meet different research needs, we provide diversified modeling pathways to ensure models align with human disease morphology and pathophysiology:
- Chemically Induced Models (Preservative-related):
- Method: Topical application of high-concentration Benzalkonium Chloride (BAC).
- Characteristics: Simulates corneal epithelial apoptosis, squamous metaplasia, and tear film disruption caused by long-term use of preservative-containing eye drops.
- Combined Environmental & Neuro-inhibition Models:
- Method: Low-humidity environment (controlled dehumidification) combined with cholinergic receptor antagonists (Scopolamine).
- Characteristics: Establishes a mixed dry eye model, significantly reducing tear secretion and simulating corneal damage in arid environments.
- Lifestyle-related Models:
- Sleep Deprivation Model: Induces increased corneal fluorescein sodium staining by interfering with animal sleep cycles.
- Blue Light Irradiation Model: Uses high-energy short-wave blue light (LED) to simulate damage caused by artificial light pollution from visual display terminals (VDTs).
- Metabolic Injury Models:
- High-Fat Diet (HFD): Induces lipid deposition and inflammation in the lacrimal gland, leading to decreased aqueous secretion.
- Diabetes Mellitus (DM) Induction: Simulates Meibomian Gland Dysfunction (MGD) and corneal hypoesthesia complicated in diabetic patients.
- Surgically Induced Models (Ocular Hypertension-related):
- Method: Episcleral vein cauterization/ligation.
- Characteristics: Observes the impact of high intraocular pressure (IOP) on the corneal endothelium and ocular surface blood supply while studying glaucomatous optic neuropathy.
Key Monitoring Indicators
- Clinical Sign Observation:
- Slit-lamp Examination: Observing corneal transparency, neovascularization, and eyelid status.
- Corneal Fluorescein Sodium Staining (FL): Evaluating the degree of corneal epithelial defects and repair speed.
- Schirmer Test: Assessing lacrimal gland function (tear secretion volume).
- Histopathological Analysis:
- HE Staining: Observing morphological changes in corneal layers, conjunctiva, and lacrimal glands.
- PAS Staining: Counting conjunctival goblet cells to evaluate ocular surface lubrication.
- IHC/IF: Detecting inflammatory cytokines (CD4+, Ly6g, F4/80), apoptosis markers, and collagen expression.
- Functional Evaluation:
- Electroretinogram (ERG): Assessing visual function for models involving optic nerve damage.
- Biochemical Testing: Measuring tear osmolarity and lipid peroxidation markers.
