Objective: To study the effects of Ginkgo biloba extract (GBE) on dexamethasone (DEX)-induced ocular hypertension.
Methods: Rabbits aged 7 weeks received topical TobraDEX (Alcon Labs, Hünenberg, Switzerland) and/or 5 microg of GBE four times daily for 14 days. Intraocular pressure (IOP) was recorded every 3 days. After enucleation, trabecular meshwork (TM) cellularity and extracellular matrix deposition were graded. The effect of GBE on apoptosis and expression of myocilin and cell stress-related genes in DEX-treated human TM cells were studied by immunofluorescence, Western blotting, and quantitative polymerase chain reaction.
Results: Ginkgo biloba extract suppressed DEX-induced IOP elevation in rabbits. It reduced the DEX-associated accumulation of extracellular materials within the cribriform layers of the TM and achieved better TM cellularity. In cultured human TM cells, GBE substantially attenuated anti-Fas ligand-induced apoptosis and reduced DEX-induced myocilin expression. Ginkgo biloba extract modulated the expression of alphaB-crystallin and heat-shock proteins 70 and 90alpha but not other stress-related genes. Furthermore, changes associated with DEX were found less in GBE-treated or GBE-primed TM cells.
Conclusion: We showed that GBE, a nontoxic, antiapoptotic, herbal compound significantly suppressed steroid-induced IOP elevation in rabbits and it seems to prevent the adverse effects of DEX on TM cells.
Clinical relevance: Ginkgo biloba extract could be a therapeutic agent or dietary supplement to prevent steroid-induced ocular hypertension.