Retinal protective effects of topically administered agmatine on ischemic ocular injury caused by transient occlusion of the ophthalmic artery

S. Hong, H. Hara, M. Shimazawa, K. Hyakkoku, C. Y. Kim, G. J. Seong

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Agmatine, an endogenous polyamine and putative neuromodulator, is known to have neuroprotective effects on various neurons in the central nervous system. We determined whether or not topically administered agmatine could reduce ischemic retinal injury. Transient ocular ischemia was achieved by intraluminal occlusion of the middle cerebral artery of ddY mice (30-35 g) for 2 h, which is known to also induce occlusion of the ophthalmic artery. In the agmatine group (N = 6), a 1.0 mM agmatinecontaining ophthalmic solution was administered four times daily for 2 weeks before occlusion. In the control group (N = 6), a 0.1% hyaluronic acid ophthalmic solution was instilled at the same times. At 22 h after reperfusion, the eyeballs were enucleated and the retinal sections were stained by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Transient ocular ischemia induced apoptosis of retinal cells in the entire retinal layer, and topically administered agmatine can significantly reduce this ischemic retinal injury. The proportion of apoptotic cells was definitely decreased (P < 0.001; Kruskal-Wallis test). Overall, we determined that topical agmatine application effectively decreases retinal damage in an in vivo ocular ischemic injury model. This implies that agmatine is a good candidate as a direct neuroprotective agent for eyes with ocular ischemic diseases.

Original languageEnglish
Pages (from-to)212-215
Number of pages4
JournalBrazilian Journal of Medical and Biological Research
Volume45
Issue number3
DOIs
Publication statusPublished - 2012 Mar 1

Fingerprint

Agmatine
Ophthalmic Artery
Eye Injuries
Ophthalmic Solutions
Neuroprotective Agents
Ischemia
Cells
DNA Nucleotidylexotransferase
Eye Diseases
Middle Cerebral Artery Infarction
Wounds and Injuries
Polyamines
Neurology
Hyaluronic Acid
Labeling
Neurons
Reperfusion
Neurotransmitter Agents
Central Nervous System
Apoptosis

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Neuroscience(all)
  • Biochemistry
  • Physiology
  • Immunology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Cell Biology

Cite this

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abstract = "Agmatine, an endogenous polyamine and putative neuromodulator, is known to have neuroprotective effects on various neurons in the central nervous system. We determined whether or not topically administered agmatine could reduce ischemic retinal injury. Transient ocular ischemia was achieved by intraluminal occlusion of the middle cerebral artery of ddY mice (30-35 g) for 2 h, which is known to also induce occlusion of the ophthalmic artery. In the agmatine group (N = 6), a 1.0 mM agmatinecontaining ophthalmic solution was administered four times daily for 2 weeks before occlusion. In the control group (N = 6), a 0.1{\%} hyaluronic acid ophthalmic solution was instilled at the same times. At 22 h after reperfusion, the eyeballs were enucleated and the retinal sections were stained by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Transient ocular ischemia induced apoptosis of retinal cells in the entire retinal layer, and topically administered agmatine can significantly reduce this ischemic retinal injury. The proportion of apoptotic cells was definitely decreased (P < 0.001; Kruskal-Wallis test). Overall, we determined that topical agmatine application effectively decreases retinal damage in an in vivo ocular ischemic injury model. This implies that agmatine is a good candidate as a direct neuroprotective agent for eyes with ocular ischemic diseases.",
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Retinal protective effects of topically administered agmatine on ischemic ocular injury caused by transient occlusion of the ophthalmic artery. / Hong, S.; Hara, H.; Shimazawa, M.; Hyakkoku, K.; Kim, C. Y.; Seong, G. J.

In: Brazilian Journal of Medical and Biological Research, Vol. 45, No. 3, 01.03.2012, p. 212-215.

Research output: Contribution to journalArticle

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AU - Hara, H.

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