[关键词]
[摘要]
目的:研究细胞间黏附分子-1(ICAM-1)在糖尿病性白内障发病机制中的作用及转化生长因子β-1(TGF-β1)对晶状体上皮细胞ICAM-1表达的影响。方法:SD大鼠120只随机分为对照组和糖尿病性白内障组。在糖尿病性白内障组中,建立糖尿病模型,免疫组织化学SP法观察两组晶状体上皮细胞中ICAM-1表达变化;RT-PCR法检测TGF-β1和TGF-β1中和抗体对体外培养的人晶状体上皮细胞ICAM-1mRNA表达的影响。结果:在糖尿病性白内障组大鼠晶状体上皮细胞ICAM-1的表达明显增高,且随着病程发展呈进行性增强,与对照组比较差异有统计学意义(P<0.01)。TGF-β1培养组的人晶状体上皮细胞的ICAM-1的表达则显著增强,与正常血清培养组比较差异具有统计学意义(P<0.05)。在TGF-β1抗体培养组中,ICAM-1的表达明显受到抑制,与TGF-β1培养组比较,差别具有统计学意义(P<0.05)。结论:TGF-β1可以促进晶状体上皮细胞ICAM-1的表达;ICAM-1通过促进晶状体上皮细胞的黏附、增殖而在糖尿病性白内障的发生中发挥重要作用。
[Key word]
[Abstract]
AIM:To evaluate the role of intercellular adhesion molecule-1(ICAM-1) in the pathogenesis of diabetic cataract,and to investigate the effects of transforming growth factorβ-1(TGF - β1) on the expression of ICAM-1 in the lens epithelium cells.METHODS:Totally 120 SD rats were randomly divided into two groups:normal control group and diabetic cataract group.Diabetic model was built in diabetic cataract group.Immunohistochemical streptavidin-peroxidases(SP) method was used to observe changes of the expression of ICAM-1 in the lens epithelium cells in two groups.RT-PCR method was used to detect the effects of TGF-β1 and TGF-β1 antibody on the expression of ICAM-1 in the cultured human lens epithelium cells.RESULTS:The expression of ICAM-1 in the lens epithelium cells was significantly higher in diabetic cataract group than that in normal control group,and increasing with the development of disease (P<0.01).The expression of ICAM-1 in the lens epithelium cells was significantly increased in TGF-β1 cultured group,which had statistical significance compared with normal serum cultured group(P<0.05).The expression of ICAM-1 was significantly inhibited in TGF-β1 antibody cultured group,which had statistical significance compared with TGF-β1 cultured group(P<0.05).CONCLUSION:TGF-β1 could induce the expression of ICAM-1 in the lens epithelium cells,and played an important role in the occurence of diabetic cataract through promoting attachment and proliferation of lens epithelium cells.
[中图分类号]
R776.1
[基金项目]
中国福建省卫生厅青年科研基金资助项目(No.2005-2-37)~~