摘要
目的检测NFκBp65、NOS2在维生素A缺乏干眼模型兔角膜中的表达和改变,探讨干眼的发病机制。方法实验组6只兔以维生素A完全缺乏饲料喂养6个月制作维生素A缺乏干眼兔模型,正常对照组6只兔喂养正常饲料,采用免疫组织化学SP方法,对模型兔和对照兔角膜组织中NFκBp65、NOS2的表达进行检测。结果与正常对照组相比,实验组维生素A缺乏干眼模型兔角膜组织中NFκBp65、NOS2的表达明显增多(P<0.01),NFκBp65在细胞中表达明显,NOS2在间质中表达明显。结论维生素A缺乏兔角膜组织中的免疫炎症反应可能是导致干眼的主要病理过程,NFκBp65、NOS2在此过程中起重要作用。
Objective Xerophthalmia is common and frequently-occurring in clinic,and its cause is comprehensive. This paper aimed to detect the expression and alteration of NFkBp65 and inducible nitric oxide synthase （NOS2） in cornea with experimental xerophthalmia and investigate the pathogenesis of xerophthalmia. Methods Experimental xerophthalmia model was induced in 6 rabbits by raising with casein-base vitamin A-deficient diet for six months and the criteria of xerophthalmia was identified based on Schirmer I test,tear film break-up time（BUT） and fluorescence score of cornea. Six control rabbits were fed with normal forage and matched environment. Corneas were removed from the rabbit models and normal controls after six months for HE stain and immunohistochemistry to detect the expressions of NFkBp65 and NOS2 in cornea. Results The fluorescence stain showed the corneal ulceration with the score 〉 1 in model rabbits,and the values of Schirmer I and BUT were significantly decreased（6.17 mm ± 1.75 mm,5.83 s ±1.95 s, respectively） in comparison with normal rabbits （30.08 mm± 6. 65 mm, 29.75 s±5.66 s） （t = 12.05,13.84,P 〈0.01）. The expression of NFkBp65 and NOS2 in the models （34.75±9.49,21. 17± 5.44 respectively） was prominently higher than that in the normal controls （4.33 ± 2.64,2.25 ± 1.76 （ t = 4.38,4.68, P 〈0. 01）. NFkBp65 was expressed mainly inside of cell and that of NOS2 was outside of cell. Conclusion The immunological inflammation may be one of the most important mechanisms leading to the destruction of cornea with xerophthalmia,and overexpression of NFkBp65 and NOS2 plays a role during the process of xerophthalmia.
出处
《眼科研究》
CSCD
北大核心
2009年第1期19-22,共4页
Chinese Ophthalmic Research
