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Int J Ophthalmol. 2011;4(4):343-8. doi: 10.3980/j.issn.2222-3959.2011.04.03. Epub 2011 Aug 18.

Potential involvement of nitric oxide synthase but not inducible nitric oxide synthase in the development of experimental corneal neovascularization.

Author information

  • 1Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.

Abstract

AIM:

To investigate the effect of nitric oxide and its synthetase on experimental corneal neovascularization (CRNV).

METHODS:

CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG). The inhibitory effect was detected at day 2 and 4 after corneal alkali injury by reverse transcription polymerase chain reaction (RT-PCR). CRNV was compared between the control and the treated mice by microscopic observation and corneal whole mount CD31 immunostaining.

RESULTS:

The inhibition of L-NAME to NOS and AG to iNOS after corneal injury was confirmed by RT-PCR (P<0.05). Compared with control mice, L-NAME treated mice exhibited significantly decreased CRNV areas (P<0.05). In contrast, AG treatment failed to attenuate alkali induced CRNV (P>0.05).

CONCLUSION:

Our findings suggest that NOS but not iNOS plays a critical role in alkali injury induced CRNV.

KEYWORDS:

corneal neovascularization; inducible nitric oxide synthase; nitric oxide synthase

PMID:
22553677
[PubMed]
PMCID:
PMC3340862
Free PMC Article
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