December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Protection of Ischemia-Reperfusion Induced Cell Death by Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in the Rat Retina
Author Affiliations & Notes
  • S-M Choi
    Lab of Ophthalmol & Visual Sci Catholic Medical Univ Seoul Republic of Korea
  • J-S Choi
    Lab of Ophthalmol & Visual Sci Catholic Medical Univ Seoul Republic of Korea
  • M-O Park
    Lab of Ophthalmol & Visual Sci Catholic Medical Univ Seoul Republic of Korea
  • B-J Gwag
    Department of Pharmacol School of Medicine Ajou Univ Suwon Republic of Korea
  • C-K Joo
    Lab of Ophthalmol & Visual Sci Catholic Medical Univ Seoul Republic of Korea
  • Footnotes
    Commercial Relationships   S. Choi, None; J. Choi, None; M. Park, None; B. Gwag, None; C. Joo, None. Grant Identification: Support: MOHW Grant 01-PJ1-PG3-21300-0012
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 770. doi:
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      S-M Choi, J-S Choi, M-O Park, B-J Gwag, C-K Joo; Protection of Ischemia-Reperfusion Induced Cell Death by Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2002;43(13):770.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: The degeneration of retinal neurons results in loss of vision. It has been known that Non Steroidal Anti-Inflammatory Drugs (NSAIDs) can protect the neuron from ischemic damage. The purpose of this study was to investigate the protective effect of NSAIDs in the rat retinal ischemia. Methods: Retinal ischemia in Sprague Dawley rats was induced by high intraocular pressure at 160 mmHg for 60 minutes after intra-ocular injection of saline, aspirin (5 to 20 mM), sulfasalazine (1 to 5 mM) or sulindac (0.01 to 0.1 mM). For morphological study, the retinas were embedded in epon 24 hours after ischemic injury. To determine neuronal survivorship in the retinal layers, the number of viable neurons was counted in 100µm X 25µm square and examined. Results: The intravitreal injections of aspirin, sulfasalazine or sulindac attenuated the ischemic neuronal degeneration in dose dependent. The protective effect of aspirin at concentration of 20 mM was observed to be 73%5.4 and 80%2.5 in ganglion cell layer (GCL) and inner nuclear cell layer (INL), respectively. Treatment with 5 mM of sulfasalazine showed the protective effect of 53%8.8 in GCL and 74%5.3 in INL whereas 65%9.4 in GCL and 84%3.0 in INL were observed for 0.1 mM of sulindac treated group. Conclusion: These data suggest that NSAIDs (aspirin, sulfasalazine or sulindac) can be the potential drugs to protect the retina neurons injured by ischemia.

Keywords: 554 retina • 448 ischemia • 489 neuroprotection 
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