[1]包永琴,马景学,杜颖华,等.二十碳五烯酸对大鼠角膜新生血管血管内皮生长因子及其受体表达的抑制作用[J].陆军军医大学学报(原第三军医大学学报),2010,32(19):2066-2070.
 Bao Yongqin,Ma Jingxue,Du Yinghua,et al.Inhibitory effect of eicosapentaenoic acid on expression of vascular endothelial growth factor and its receptor Flk-1 in corneal neovascularization of rats[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(19):2066-2070.
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二十碳五烯酸对大鼠角膜新生血管血管内皮生长因子及其受体表达的抑制作用(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
32卷
期数:
2010年第19期
页码:
2066-2070
栏目:
论著
出版日期:
2010-10-15

文章信息/Info

Title:
Inhibitory effect of eicosapentaenoic acid on expression of vascular endothelial growth factor and its receptor Flk-1 in corneal neovascularization of rats
作者:
包永琴马景学杜颖华王淑芬
河北医科大学第二医院眼科
Author(s):
Bao Yongqin Ma Jingxue Du Yinghua Wang Shufen
Department  of  Ophthalmology, Second Hospital  of  Hebei  Medical  University, Shijiazhuang, Hebei Province, 050000, China
关键词:
角膜新生血管化二十碳五烯酸血管内皮生长因子血管内皮生长因子受体2
Keywords:
corneal neovascularization eicosapentaenoic acid vascular endothelial growth factor Flk-1
分类号:
R779.1; R977.6; R322.13
文献标志码:
A
摘要:
目的 探讨二十碳五烯酸(eicosapentaenoic acid, EPA)对大鼠角膜新生血管(corneal neovascularization, CNV)血管内皮生长因子(VEGF)及其受体Flk-1表达的影响及作用机制。  方法  78只SD大鼠按随机数字表法分为碱烧伤0.02 mg EPA治疗组(A组, 24只)、碱烧伤0.03 mg EPA治疗组(B组, 24只)、碱烧伤对照组(C组, 24只)、正常组(D组, 6只), 除正常组外,均选用右眼制作碱烧伤模型。A、B、C组碱烧伤后立即分别球结膜下注射0.02 mg/0.04 ml EPA、0.03 mg/0.04 ml EPA、0.04 ml生理盐水。每日裂隙灯显微镜下观察角膜水肿、新生血管情况。碱烧伤后1、4、7、14 d,用免疫组织化学方法检测角膜新生血管内皮细胞CD34表达,用逆转录聚合酶链反应(RT-PCR)及蛋白印迹法分别检测角膜VEGF的mRNA表达及Flk-1的蛋白表达。 结果   碱烧伤7 d和14 d,角膜新生血管相对面积A组:(15.80±6.43)%、(11.06±2.14)%, B组:(16.10±7.41)%、(11.06±2.51)%,均显著少于C组:(84.74±7.77)%、(89.63±7.50)% (P<0.05)。碱烧伤后7 d,C组CD34在CNV内皮细胞强阳性表达,A、B组未见CNV内皮细胞,CD34无表达。C组Flk-1蛋白及VEGF的mRNA表达,碱烧伤后1 d最高,持续高表达至4 d,随后逐渐下降。碱烧伤4 d,A、B组VEGF的mRNA表达及Flk-1的蛋白表达显著低于C组(P<0.05)。 结论   EPA能通过VEGF途径,抑制VEGF及其受体Flk-1的表达,从而显著抑制角膜新生血管的生长。
Abstract:
Objective   To study the effect of eicosapentaenoic acid (EPA) on expression of vascular endothelial growth factor (VEGF) and its receptor Flk-1 in corneal neovascularization (CNV) of rats and its mechanism of action.  Methods   Seventyeight SprayueDawley rats were randomly divided into group A treated with 0.02 mg EPA (n=24), group B treated with 0.03 mg EPA (n=24), group C (control group, n=24), and group D (normal group, n=6). A model of right eye injury was induced by alkali cauterization. A solution containing 0.02 mg/0.04 ml and 0.03 mg/0.04 ml of EPA and 0.04 ml of saline was injected subconjunctivally in groups A, B and C immediately after alkali cauterization. CNV and corneal edema were observed daily under a slitlamp biomicroscope. On days 1, 4, 7 and 14 after operation, vascular endothelial cells were stained with CD34 using immunohistochemical method. VEGF mRNA and Flk-1protein expressions were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis.  Results    The relative area of CNV in groups A and C was 15.80%±6.43% and 11.06%±2.14%, 16.10%±7.41% and 11.06%±2.51%, 84.74%±7.77% and 89.63%±7.50%, respectively, in 7 and 14 d after injury induced by alkali cauterization. The relative area of CNV was significantly lower in groups A and B than in control group in 7 and 14 d after injury induced by alkali cauterization (P<0.05). The vascular endothelial cells in corneal stroma of group C were strongly stained with CD34 and the endothelial marker was negatively stained in EPA-treated avascular stroma. The VEGF mRNA and Flk-1 protein expression levels were the highest in groups C in 1 and 4 d after injury induced by alkali cauterization, and then decreased, and were significantly lower in groups A and B than in control group in 4 d after injury induced by alkali cauterization (P<0.05).  Conclusion   Topical application of EPA can inhibit the expression of VEGF and its receptor Flk-1 through the VEGF pathway, thus significantly suppressing CNV.

相似文献/References:

[1]张侃,曾琳,龙在云,等.必需脂肪酸对大鼠脑组织中EPA、DHA含量的影响及意义[J].陆军军医大学学报(原第三军医大学学报),2005,27(12):1213.

更新日期/Last Update: 2010-10-08