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大鼠模型中抗坏血酸对角膜血管生成的抑制作用。

Inhibition of corneal angiogenesis by ascorbic acid in the rat model.

作者信息

Peyman Gholam A, Kivilcim Muhamet, Morales Ana Munoz, DellaCroce John T, Conway Mandi D

机构信息

Department of Ophthalmology, University of Arizona, Arizona Health Sciences Center, 655 N. Alvernon Way, Suite 108, Tucson, AZ 85711, USA.

出版信息

Graefes Arch Clin Exp Ophthalmol. 2007 Oct;245(10):1461-7. doi: 10.1007/s00417-007-0542-4. Epub 2007 Feb 21.

DOI:10.1007/s00417-007-0542-4
PMID:17318569
Abstract

PURPOSE

To evaluate the effect of topically administered ascorbic acid on experimentally induced corneal neovascularization in the rat model.

MATERIALS AND METHODS

Corneal chemical cauterization of 72 eyes in Long-Evans male rats was performed using silver nitrate/potassium nitrate sticks. Nine groups of eight eyes were used to evaluate eight concentrations of ascorbic acid with one group of eight eyes serving as a control. Topical instillation of 100 mg/ml non-pH-neutralized ascorbic acid was performed in one group while the remaining seven groups were evaluated using pH-neutralized ascorbic acid in concentrations of 100 mg/ml, 50 mg/ml, 10 mg/ml, 5 mg/ml, 1 mg/ml, 500 microg/ml, and 250 microg/ml.

RESULTS

The percentage of corneal neovascularization and burn stimulus score was determined for all the eyes. The means of percent of corneal neovascularization in ascorbic acid 100 mg/ml (non-neutralized), 100 mg/ml, 50 mg/ml, 10 mg/ml, 5 mg/ml, 1 mg/ml, 500 microg/ml, 250 microg/ml, and control group were 17.50 +/- 12.80 (p = 0.001), 17.00 +/- 19.30 (p = 0.001), 15.25 +/- 13.26 (p = 0.001), 17.62 +/- 11.89 (p = 0.001), 28.87 +/- 23.08 (p = 0.001), 29.62 +/- 16.91 (p = 0.001), 60.12 +/- 8.50 (p = 0.04), 65.62 +/- 2.26 (p = 0.185), and 68.25 +/- 4.06, respectively (Tables 1 and 2). All animals had a burn score of 2+ or higher (Table 1).

CONCLUSION

Ascorbic acid applied in a topical solution appears to inhibit corneal neovascularization in the rat model of inflammatory neovascularization in concentrations in a dose-dependent manner. The optimal dose-effect relation was in our model found in concentrations between 1 mg and 500 microg/ml. At concentrations below 500 microg/ml there was no statistically significant inhibition in the degree of corneal neovascularization compared to control.

摘要

目的

评估局部应用抗坏血酸对大鼠实验性诱导角膜新生血管形成的影响。

材料与方法

使用硝酸银/硝酸钾棒对Long-Evans雄性大鼠的72只眼睛进行角膜化学烧灼。九组,每组八只眼睛,用于评估八种浓度的抗坏血酸,一组八只眼睛作为对照。一组局部滴注100mg/ml未调节pH值的抗坏血酸,其余七组使用pH值调节后的抗坏血酸,浓度分别为100mg/ml、50mg/ml、10mg/ml、5mg/ml,、1mg/ml、500μg/ml和250μg/ml。

结果

测定了所有眼睛的角膜新生血管形成百分比和烧伤刺激评分。抗坏血酸100mg/ml(未中和)、100mg/ml、50mg/ml、10mg/ml、5mg/ml、1mg/ml、500μg/ml、250μg/ml组和对照组的角膜新生血管形成百分比平均值分别为17.50±12.80(p = 0.001)、17.00±19.30(p = 0.001)、15.25±13.26(p = 0.001)、17.62±11.89(p = 0.001)、28.87±23.08(p = 0.001)、29.62±16.91(p = 0.001)、60.12±8.50(p = 0.04)、65.62±2.26(p = 0.185)和68.25±4.06(表1和表2)。所有动物的烧伤评分为2+或更高(表1)。

结论

在局部溶液中应用抗坏血酸似乎以剂量依赖的方式抑制大鼠炎症性新生血管形成模型中的角膜新生血管形成。在我们的模型中,最佳剂量效应关系出现在1mg至500μg/ml的浓度之间。与对照组相比,浓度低于500μg/ml时,角膜新生血管形成程度没有统计学上的显著抑制。

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