title: Changes of the Retina and Intrinsic Survival Signals in a Rat Model of Glaucoma following Brinzolamide and Travoprost Treatments.
abstract: OBJECTIVE
  The purpose of this study is to examine the changes of the retina and the intrinsic survival signals of the retina by brinzolamide (Azopt®) and travoprost (Travatan®) in a rat model of chronic ocular hypertension.
  
  
  METHODS
  Chronic ocular hypertension was induced by cauterization of three episcleral veins. Terminal deoxynucleotidyl transferase-mediated dUTP-nick end-labeling (TUNEL) staining was performed and the expression of glial fibrillary acidic protein (GFAP) was examined to evaluate changes of retinal ganglion cell (RGC) apoptosis and glial cell activation. Western blot analyses of the bcl-2 family and extracellular signal-regulated kinases (ERK) were done to identify changes of the intrinsic survival signaling pathway in the retina.
  
  
  RESULTS
  GFAP expression and TUNEL staining revealed significant decreases in RGC apoptosis and glial cell activation after brinzolamide and travoprost administration; bcl-2 and bcl-xL expression were significantly increased after intraocular pressure elevation and it was further increased with brinzolamide and travoprost treatment. This enhancement of survival signaling may have contributed to the decrease in RGC apoptosis. However, the role of ERK signaling was not significant.
  
  
  CONCLUSIONS
  Decrease in retinal damage and increased intrinsic survival signals suggests the neuroprotective potential of brinzolamide and travoprost in an animal model of chronic ocular hypertension, but further studies are required.
authors.affiliation: Department of Ophthalmology and Visual Science, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Hae Young Lopilly
authors.initials: HY
authors.lastname: Park
authors.forename: Jie Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Dong Eun
authors.initials: DE
authors.lastname: Lee
authors.forename: Joo Hwa
authors.initials: JH
authors.lastname: Lee
authors.forename: Chan Kee
authors.initials: CK
authors.lastname: Park
mesh_terms: D000287:Administration, Topical; D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D015153:Blotting, Western; D002257:Carbonic Anhydrase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D002470:Cell Survival; D004195:Disease Models, Animal; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D007429:Intraocular Pressure / Q000187:drug effects; D008297:Male; D009798:Ocular Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009883:Ophthalmic Solutions; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D013449:Sulfonamides / Q000008:administration & dosage / Q000627:therapeutic use*; D013843:Thiazines / Q000008:administration & dosage / Q000627:therapeutic use*; D000069557:Travoprost / Q000008:administration & dosage / Q000627:therapeutic use*; D051020:bcl-X Protein / Q000378:metabolism
chemical_list: D000959:Antihypertensive Agents; C494812:Bcl2l1 protein, mouse; D002257:Carbonic Anhydrase Inhibitors; D005904:Glial Fibrillary Acidic Protein; D009883:Ophthalmic Solutions; D019253:Proto-Oncogene Proteins c-bcl-2; D013449:Sulfonamides; D013843:Thiazines; D051020:bcl-X Protein; C111827:brinzolamide; D048049:Extracellular Signal-Regulated MAP Kinases; D000069557:Travoprost