目的:通过对比姜黄素与Avastin抑制大鼠碱烧伤后角膜新生血管(corneal neovascularization,CNV)及血管内皮生长因子(vascular endothelial growth factor,VEGF)表达水平的影响,进一步探讨姜黄素抑制CNV形成的机制.方法:选取SD大白鼠共30只,建立碱烧伤模型,随机将大鼠分成A,B两组,各15只,A组中右眼为实验组 A1组,左眼为空白对照组A2;B组中右眼为实验组B1,左眼为空白对照组B2.A1组给予40μmol/L姜黄素配置成的滴眼液,A2组滴用生理盐水;B1组给予5g/L Avastin滴眼液,B2组滴用生理盐水.根据不同时间点取角膜组织进行病理切片研究、抽取房水进行ELISA测定,计算出每视野计数微新生血管及房水中VEGF含量.对以上指标进行对比分析研究.结果:两种药物均未发现在角膜水肿、角膜修复等方面的毒副作用.对新生血管的影响,两种药物CNV计数均明显低于空白对照组(P<0.01),两种药物之间对新生血管影响的对照,平均CNV计数无显著性区别.A1组与A2组对比、B1组与B2组对比,实验组VEGF均明显低于对照组,有高度显著性统计学意义(P<0.01),A1组与B1组对照,平均VEGF含量A1组高于B1组,有统计学意义(P<0.05).结论:姜黄素的VEGF抑制能力可能不如Avastin,但在整体抗CNV的能力上并不输于Avastin,说明姜黄素还参与了干预角膜碱烧伤CNV形成的其他机制.%AIM: To compare the inhibitory effect of curcunmin and Avastin on the rat corneal neovascularization(CNV), and approach the mechanism of the curcunmin's inhibition.METHODS: CNV was established in thirty SD rats by alkaline burning. Rats were divided equally to group A and group B at random. In group A, right eyes were experimental group A1, treated by 40μmol/L curcunmin solution, and left eyes were control group A2, treated by 0. 09% sodium chloride. In group B, right eyes were experimental group group B1, treated by 5g/L avastin, and left eyes were control group B2, treated by 0. 09% sodium chloride. Cornea and aqueous humor were collected by time spot. The capillary vessels were study, and the expressions of VEGF were detected by Enzyme-Linked immunosorbnent Assay (ELISA).RESULTS: No toxic effects of the drugs were found. The capillary vessels in experimental group were less than those of control group (P<0. 01 ). No statistical different of the capillary vessels between two drugs were found. The expressions of VEGF in experimental group were less than those in control group (P<0. 01). The expressions of VEGF in B1 group were less than in group A1.CONCLUSION: The inhibitory effect to CNV of curcunmin and avastin have no statistical different in the experiment, but curcunmin has the less inhibitory effect to the expressions of VEGF than avastin. Curcunmin may have other mechanism in the inhibitory action on CNV.
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