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This dissertation, Neuroprotective Effect of Ginkgo Biloba Extract on Retinal Ganglion Cells in a Rat Glaucoma Model by Ching, Lai, 賴晴, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Neuroprotective effect of Ginkgo biloba extract on retinal ganglion cells in a rat glaucoma model submitted by Ching Lai for the degree of Master of Philosophy at the University of Hong Kong in August 2003 Glaucoma is a progressive optic neuropathy that ultimately causes retinal ganglion cell (RGC) death and loss of vision. Current therapies on this disease only aim at controlling intraocular pressure (IOP). However, patients undergoing such therapies may still develop RGCs degeneration. Therefore a new therapy has been suggested and is named neuroprotection. Neuroprotection aims at protecting and rescuing RGCs from damage. One suggested neuroprotectant is the Ginkgo biloba extract (GBE). GBE is a traditional Chinese medicine, which has been shown to increase ocular blood flow velocity and thus may improve vision. However, the direct effect of GBE on RGCs survival has not been investigated. Therefore, the objective of this study is to investigate the neuroprotective effect of GBE on RGCs in an ocular hypertension model. By using a laser-induced ocular hypertension model, we have demonstrated the neuroprotective effect of GBE on RGC survival. After administered Sprague- Dawley rats with 12 mg/ml, 120 mg/ml and 200 mg/ml GBE, RGC death observed in experimental glaucoma was virtually abolished. The possible neuroprotective mechanisms of GBE on experimental glaucoma were also examined in this study. It has been proposed that GBE protects neurons by modulating glial responses. We found that the number of OX42 immunopositive microglia was increased after GBE treatment in glaucomatous retinas. Based on the morphological analysis, the numbers of both the resting and activated forms of microglia were increased with GBE administration. The protective effect of GBE on RGCs was partially removed by inhibiting the response of microglia with the microglia inhibitory factor. We have also studied the role of other glial cells in protecting RGCs. Macroglia such as astrocytes and Muller cells were studied by quantifying the GFAP immunolabeled glial cells in the glaucomatous retina. Immunoreactivity of GFAP was enhanced after 1.2 mg/ml, 12 mg/ml and 120 mg/ml GBE treatments. In experiments on different survival periods after GBE administration, GBE was shown to induce an earlier onset and a sustained expression of GFAP in the glaucomatous retina when compared with the controls. Application of GBE may therefore be a potentially useful treatment in preventing the loss of vision in glaucoma patients. DOI: 10.5353/th_b2949405 Subjects: Retinal ganglion cellsGinkgo - Therapeutic useGlaucomaRats as laboratory animals

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