Objective: To evaluate the effect of 0.2% ambroxol eye drop on
tear secretion and corneal healing on a rabbit dry eye model, and to delineate
potential underlying mechanisms. Materials and method: A mixed
mechanism dry eye model was created using 12 healthy New Zealand rabbits
by excision of the main lacrimal glands, Harderian gland and nictitating
membrane. Establishment of the model was confirmed by the decrease of Schirmer I
and increase of corneal fluorescein staining scores. Two weeks after model
creation, the rabbits were randomly and evenly divided into NaCl, 0.1% sodium
hyaluronate and 0.2% ambroxol groups. Each group was administered the respective
eye drops 4 times a day for four weeks. The Schirmer I test and corneal
fluorescein staining were performed at two and four weeks. After four weeks of
treatment, the animals were sacrificed and the conjunctiva and eyelid specimens
collected. Inflammatory factors IL-8, TNF-, and goblet cell specific
mucin MUC5AC were measured by ELISA while the lid meibomian gland was evaluated
by oil red O staining. Results: Compared with the baseline, 2 weeks
after the surgery, Schirmer I test value decreased significantly (20.35
5.18 mm/5 min vs 13.95 4.64 mm/5 min, p 0.01), and the
fluorescein staining score increased significantly (0.5 0.6 vs 5.5
1.4, p 0.01). After four weeks of treatment, compared with
the NaCl and sodium hyaluronate groups, tear secretion in ambroxol group
increased significantly (p 0.01), while the corneal fluorescence
staining score decreased significantly (p 0.01). In the conjunctival
tissue, significant decrease was seen in TNF- (p 0.01) and
IL-8 [p (unilateral) 0.05] concentrations in ambroxol group, and
significant increase in MUC5AC concentration (p 0.01) in ambroxol
group as well. The lipid content in the lid meibomian glands appeared increased
after the administration of ambroxol. Conclusion: The present rabbit dry
eye model study demonstrated potentials of topically administered 0.2% ambroxol
in stimulating tear and mucin secretion, inhibiting ocular surface inflammation,
promoting corneal healing, and possibly augmenting meibomian gland lipid
production.