一氧化氮合酶而非诱导型一氧化氮合酶可能参与实验性角膜新生血管形成的过程。
Potential involvement of nitric oxide synthase but not inducible nitric oxide synthase in the development of experimental corneal neovascularization.
作者信息
Chen Yuan, Liu Gao-Qin, Lu Pei-Rong
机构信息
Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
出版信息
Int J Ophthalmol. 2011;4(4):343-8. doi: 10.3980/j.issn.2222-3959.2011.04.03. Epub 2011 Aug 18.
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.
目的
研究一氧化氮及其合成酶对实验性角膜新生血管化（CRNV）的影响。
方法
通过碱烧伤诱导小鼠发生CRNV，用NG-硝基-L-精氨酸（L-NAME）抑制一氧化氮合成酶（NOS），用氨基胍半硫酸盐（AG）抑制诱导型一氧化氮合成酶（iNOS）。在角膜碱烧伤后第2天和第4天，通过逆转录聚合酶链反应（RT-PCR）检测抑制效果。通过显微镜观察和角膜全层CD31免疫染色比较对照组和治疗组小鼠的CRNV情况。
结果
RT-PCR证实角膜损伤后L-NAME对NOS及AG对iNOS有抑制作用（P<0.05）。与对照小鼠相比，L-NAME治疗的小鼠CRNV面积显著减小（P<0.05）。相反，AG治疗未能减轻碱诱导的CRNV（P>0.05）。
结论
我们的研究结果表明，在碱烧伤诱导的CRNV中，起关键作用的是NOS而非iNOS。
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