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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.
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篇名 在试验性的角膜的 neovascularization 的发展的氮的氧化物 synthase 然而并非可诱导的氮的氧化物 synthase 的潜在的参与
来源期刊 国际眼科杂志:英文版 学科 医学
关键词 CORNEAL NEOVASCULARIZATION NITRIC OXIDE SYNTHASE INDUCIBLE NITRIC OXIDE SYNTHASE
年,卷(期) 2011,(4) 所属期刊栏目
研究方向 页码范围 343-348
页数 6页 分类号 R772.2
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节点文献
CORNEAL
NEOVASCULARIZATION
NITRIC
OXIDE
SYNTHASE
INDUCIBLE
NITRIC
OXIDE
SYNTHASE
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国际眼科杂志:英文版
月刊
2222-3959
西安市友谊东路269号
出版文献量(篇)
2720
总下载数(次)
2
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0
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