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目的 :研究高糖作用下近端肾小管上皮细胞c fos、c jun的表达 ,探讨c Fos/c Jun异二聚体 (活化蛋白 1,AP 1)在介导高糖致近端肾小管细胞过度合成细胞外基质 (ECM)中的作用。 方法 :采用LLC PK1细胞株 ,将细胞分为正常对照组 (NG组 ,5 5mmol/LD 葡萄糖 )及高糖组 (HG组 ,2 5mmol/LD 葡萄糖 ) ;c fos、c junmRNA检测运用半定量RT PCR法 ,蛋白检测采用细胞免疫化学法。 结果 :HG组c fos、c junmRNA分别在 1、2h出现升高 ,并分别在 12、2 4h达最高峰 ;NG组上述基因的表达均无显著改变 ;与NG组相比 ,HG组c fos、c junmRNA分别升高1 63倍、1 67倍 ;HG组c Fos蛋白水平无明显变化 ,c Jun蛋白则显著升高达 4 5 %。 结论 :高糖能促进近端肾小管细胞c fos、c jun的表达 ,并可能通过AP 1(c Fos/c Jun)的形成增加介导高糖促进ECM表达的致病作用。
AIM: To investigate the expression of c fos and c jun in proximal tubular epithelial cells induced by high glucose and to explore the role of c Fos / c Jun heterodimers (activator protein 1, AP 1) in mediating high glucose induced proximal tubular cells Over-synthesis of extracellular matrix (ECM) in the role. METHODS: LLC PK1 cells were used to divide the cells into normal control group (NG group, 5 5 mmol / L glucose) and high glucose group (HG group, 25 mmol / L glucose) PCR method, protein detection using immunocytochemistry. Results: The levels of c fos and c jun mRNA in HG group increased at 1,2 h and reached the peak at 12 and 24 h, respectively. There was no significant change in the expression of the above genes in NG group. Compared with NG group, c fos , C jun mRNA increased by 1 63 times and 1 67 times respectively. There was no significant change in c Fos protein level and c Jun protein in HG group was significantly increased 45%. CONCLUSION: High glucose can promote the expression of c fos and c jun in proximal tubular cells, and may induce the pathogenicity of high glucose-induced ECM expression through the increase of AP 1 (c Fos / c Jun) formation.