趋化因子受体CCR3拮抗剂在实验性角膜新生血管发生过程中的作用和机制  

Inhibited experimental mouse corneal neovascularization by CCR3 antagonist

作　　者：刘高勤[1] 赫雪飞[1] 周文娟[1] 肖艳辉[1] 陈志刚[1] 陆培荣[1] 

机构地区：[1]苏州大学附属第一医院眼科,215006

出　　处：《中华眼科杂志》2014年第4期285-289,共5页Chinese Journal of Ophthalmology

基　　金：国家自然科学基金面上项目（30972712,81200727）;江苏省医学重点人才项目（RC2011104）;苏州大学“博士研究生学术新人奖”计划;江苏省第四期“333高层次人才培养工程”计划

摘　　要：目的 探讨趋化因子受体CCR3拮抗剂在实验性角膜新生血管发生过程中的作用及机制.方法 实验研究.以碱烧伤法诱导实验性小鼠角膜新生血管模型;选用动物为54只7～8周龄雄性健康的BABL/c小鼠,随机数字表法分成对照组、实验组及VEGF抗体阳性对照组,每组18只;Real-time PCR法检测CCR3在碱烧伤角膜组织中的动态表达;烧伤后角膜局部应用CCR拮抗剂进行干预,在碱烧伤后2周大体观察及全角膜铺片CD31组织化学染色法检测角膜新生血管发生情况;Real-time PCR和免疫印迹法检测烧伤角膜组织内血管生成相关因子的表达.应用独立样本t检验法比较各组间差异.结果 碱烧伤后2周,CCR3拮抗剂干预组角膜新生血管相对值较对照组明显减少.对照组为0.77 ±0.15,实验组为0.51 ±0.03,差异有统计学意义（t=12.91,P =0.00）.免疫印迹检测结果显示角膜组织内VEGF的表达对照组为1.15 ±0.30,实验组为0.91 ±0.24,差异无统计学意义（t=1.08,P =0.34）.结论 CCR3信号通路阻滞后能抑制实验性角膜新生血管的发生.Objective To explore the effect of CCR3 antagonist on the development of experimental corneal neovascularization.Methods Mouse corneas were burned by NaOH to induce corneal neovascularization.Fifty four clean male BABL/c mice aged 7-8 weeks were divided into control group,CCR3 antagonist group and VEGF antibody positive group according to randomized number table.The gene expression of CCR3 and its ligand eotaxin in burned corneas was examined by Real-time PCR.CCR3 antagonist was locally administrated after alkali injury and the formation of corneal neovascular 2 weeks after injury was examined using a digital camera linked to a slit lamp microscope and corneal whole mount staining with CD31.The mRNA and protein expression of chemokines in burned corneas was detected by Real-time PCR and western blot.Results Compared to control group,CCR3 antagonist treated mice resulted in significantly decreased corneal neovascularization.The related CNV area was 0.51 ± 0.03 in the CCR3 antagonist group,and that in the control group was 0.77 ± 0.15,with significant difference between them （t =12.91,P =0.00）.Western blot detection did not show significant difference of VEGF protein expression between two groups.Expression level of VEGF in the CCR3 antagonist group was 0.91 ± 0.24,and that in the control group was 1.15 ± 0.30,showing no significant difference （t =1.08,P =0.34）.Conclusions Alkali-induced corneal neovascularization was inhibited by CCR3 antagonist.The mechanism that CCR3 pathway plays an important role in corneal neovascularization needs further exploration.

关 键 词：角膜新生血管化 受体 CCR3 烧伤 化学 眼烧伤 

分 类 号：R772.2[医药卫生—眼科]