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Li-Yun Jia, PhD; Ling Sun, BSc; Dorothy S. P. Fan, FRCS; Dennis S. C. Lam, MD; Chi Pui Pang, DPhil; Gary H. F. Yam, PhD

Arch Ophthalmol. 2008;126(12):1700-1706.

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 µg 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 B-crystallin and heat-shock proteins 70 and 90 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.

Author Affiliations: Department of Ophthalmology and Visual Sciences, Chinese University of Hong Kong, Hong Kong (Drs Jia, Fan, Lam, Pang, and Yam and Ms Sun); Joint Shantou International Eye Center of Shantou University, Shantou, China (Ms Sun and Drs Lam and Pang).

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