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Abstract #22922 Published in IGR 11-1
Intraocular pressure lowering, change of antiapoptotic molecule expression, and neuroretinal changes by dorzolamide 2%/timolol 0.5% combination in a chronic ocular hypertension rat model
Park HY; Lee NY; Kim JH; Park CKJournal of Ocular Pharmacology and Therapeutics 2008; 24: 563-571
The aim of this study was to examine intraocular pressure lowering, change of antiapoptotic molecules expression, and neuroretinal changes by a commercially available dorzolamide 2%/timolol 0.5% combination in a chronic ocular hypertension rat model. Chronic ocular hypertension was induced by three episcleral vein cauterizations. The expression of antiapoptotic molecules and the effect of dorzolamide 2%/timolol 0.5% combination in chronic ocular hypertensive retina were evaluated. Retinal ganglion cell (RGC) retrograde labeling and quantification with 4-di-10-ASP (DiA) and expression of glial fibrillary acidic protein (GFAP) were detected before and after the administration of dorzolamide 2%/timolol 0.5%. Treatment of ocular hypertensive eyes with dorzolamide 2%/timolol 0.5% significantly reduced, intraocular pressure when compared to the control eyes. Labeling of RGCs with DiA showed a significant decrease in RGC loss after the administration of dorzolamide 2%/timolol 0.5%. GFAP expression revealed a significant decrease in retinal damage after dorzolamide 2%/timolol 0.5% administration. However, dorzolamide 2%/timolol 0.5% did not affect Bcl-2 and Bcl-xL mRNA expression. In conclusion, dorzolamide 2%/timolol 0.5% may have neuroprotective potential in the animal model, which is not mediated by Bcl-2 or Bcl-xL. The mechanism of neuroprotection by dorzolamide 2%/timolol 0.5% in chronic glaucoma models requires further investigation.
Dr. C.K. Park, Department of Ophthalmology and Visual Science, St. Mary's Hospital, Catholic University of Korea, 505 Banpo-dong, Seocho-ku, Seoul 137-701, South Korea. ckpark@catholic.ac.kr
Classification:
11.13.2 Betablocker and carbon anhydrase inhibitor (Part of: 11 Medical treatment > 11.13 Combination therapy)
11.8 Neuroprotection (Part of: 11 Medical treatment)
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)