中文摘要：

目的该研究观察在糖基化终末产物（AGEs）诱导大鼠肾小球系膜细胞（GMCs）中,心肌素相关转录因子MRTFA的变化及其对细胞黏附分子（ICAM-1）及纤维连接蛋白（FN）的影响,探讨MRTF-A是否通过影响NF-κB信号通路参与糖尿病肾病。方法 AGEs条件下,抑制剂CCG-1423抑制MRTF-A,或对MRTF-A进行过表达,干扰处理,通过Western blot检测MRTF-A、ICAM-1和FN的蛋白水平变化及p65在细胞核内的水平。结果在AGEs诱导的GMCs中,MRTF-A的蛋白表达增加;干扰或抑制MRTF-A能够下调AGEs诱导的FN和ICAM-1的蛋白表达及p65入核水平;而过表达MRTF-A则进一步上调FN和ICAM-1的蛋白表达及p65入核水平。结论 AGEs能够上调GMCs中MRTF-A的表达,且MRTF-A通过影响NF-κB信号通路参与介导了AGEs诱导的FN和ICAM-1的蛋白表达。

英文摘要：

Aim To observe the expression of MRTF-A in rat glomerular mesangial cells（ GMCs） induced by advanced glycation end products（ AGEs） and its effect on ICAM-1 and FN;to explore whether MRTF-A is involved in the process of diabetic nephropathy by affecting NF-κB pathway.Methods Under the condition of AGEs,CCG-1423 and anti-MRTF-A small interfering RNA were used to knock down MRTF-A and MRTF-A plasmid was used to activatt MRTF-A,The expression level of MRTF-A,ICAM-1,FN and p65 in nucleus were detected by Western blot.Results The protein expressions of MRTF-A was increased in AGEs-induced GMCs.The expressions of FN and ICAM-1 and p65 in nucleus were downregulated by knocking down MRTF-A.However,the expressions of FN,ICAM-1and p65 in nucleus were upregulated by overexpressing MRTF-A.Conclusions AGEs can upregulate the expression of MRTF-A in GMCs,and MRTF-A mediates the protein expressions of FN and ICAM-1 by affecting NF-κB signaling pathway in AGEs-induced GMCs.