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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
【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。
【Abstract】 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.
【Key words】 AGEs; Basic fibroblast growth factor; Müller cell; Diabetic retinoopathy;
- 【文献出处】 中国免疫学杂志 ,Chinese Journal of Immunology , 编辑部邮箱 ,2015年12期
- 【分类号】R774.1
- 【被引频次】1
- 【下载频次】80