糖基化终末产物对培养的兔视网膜Müller细胞bFGF表达的影响  

Effect of advanced glycosylation end products on bFGF expression of cultured rabbit Müller cells

作　　者：冷瀛[1] 王越晖[2] 张达宁[1] 李相军[1] 白丹[1] 

机构地区：[1]北华大学附属医院眼科,吉林132011 [2]吉林大学第一医院老年病科,长春130021

出　　处：《中国免疫学杂志》2015年第12期1621-1623,1632,共4页Chinese Journal of Immunology

基　　金：吉林省科技厅科技引导计划资助项目(20120749);吉林省教育厅科技研究项目(2014169);吉林省卫生厅科研课题(2011z097)资助

摘　　要：目的:观察在不同剂量糖基化终产物(AGEs)条件下,对体外培养的视网膜Müller细胞碱性成纤维生长因子(b FGF)表达的影响及其机制。方法:采用免疫细胞化学及透射电镜方法鉴定体外培养的兔视网膜Müller细胞;应用免疫细胞化学方法半定量观察640μl/2 000μl AGEs条件下视网膜Müller细胞b FGF表达的变化;利用RT-PCR技术观察AGEs、PKC抑制剂Calphostin C对视网膜Müller细胞b FGF mRNA表达的影响。结果:640μl/2 000μl AGEs可刺激视网膜Müller细胞表达b FGF,Calphostin C可明显抑制AGEs引起的b FGF mRNA表达的增加,在浓度为50 nmol/L时其抑制作用最强。结论:AGEs刺激Müller细胞b FGF的表达,发挥促血管生成的作用,b FGF mRNA的表达可能是通过激活PKC途径实现的。Objective： To observe the effects of different doses of advanced glycosylation end products（ AGEs） on b FGF expression of cultured rabbit Müller cells in vitro. Methods： Immunocytochemistry and transmission electron microscopy methods were used identified cultured Müller cell. Immunocytochemistry method was used to semi-quantitate b FGF expression of retinal Müller cells at640 μl /2 000 μl AGEs conditions. We observed effects of AGEs and PKC inhibitor Calphstion C on b FGF mRNA expression. Results：640 μl /2 000 μl AGEs stimulate b FGF expression of retinal Müller cell. Calphostin C inhibits b FGF mRNA increase stimulated by AGEs,and inhibition achieves strongest at concentration 50 nmol / L. Conclusion： AGEs can stimulate b FGF expression of Müller cell to exert the role of angiogenesis. b FGF mRNA expression may be regulated by activation of PKC pathway.

关 键 词：AGES 碱性成纤维生长因子 MÜLLER细胞 糖尿病视网膜病变 

分 类 号：R774.1[医药卫生—眼科]