摘要
目的观察全反式维甲酸(ATRA)对高糖诱导人肾小管上皮细胞(HK-2)纤维连接蛋白(FN)、层粘连蛋白(LN)表达的影响,探讨ATRA延缓糖尿病肾病肾间质纤维化的发生机制。方法体外培养的HK-2细胞随机分为正常对照组(NG组,含5.5mmol/LD-glucose);高糖组(HG组,含30mmol/LD-glucose);渗透压对照组(MG组,含5.5mmol/LD-glucose+24.5mmol/Lmannitol);全反式维甲酸低浓度组(ATRA1组,HG+10-7mol/LATRA);全反式维甲酸中浓度组(ATRA2组,HG+10-6mol/LATRA);全反式维甲酸高浓度组(ATRA3组,HG+10-5mol/LATRA);药物溶剂无水乙醇组(HG+10-2mol/L无水乙醇);卡托普利组(HG+10-5mol/Lcaptopril)。各组细胞分别培养24h、48h和72h后收集细胞上清液。采用酶联免疫吸附法(ELISA)检测培养细胞上清液FN、LN的浓度。结果高糖可增加HK-2细胞培养上清的FN、LN的水平(P<0.01),ATRA可以部分抑制高糖的作用(P<0.01)。结论高糖可以促进体外培养的HK-2细胞FN、LN的表达,ATRA可以抑制高糖的作用,这可能是ATRA延缓糖尿病肾病肾间质纤维化进展的机制之一。
Objective To investigate the effects of all-trans retinoic acid on the expression of Fibronectin（FN） and Laminin（LN） in human renal tubular epithelial cells（HK-2） so as to explore the role of all-trans retinoic acid on the pathogenesis of delaying renal interstitial fibrosis.Methods HK-2 cells cultured in vitro were divided randomly into eight groups：normal glucose group with 5.5 mM D-glucose（NG）;high glucose group with 30 mM D-glucose（HG）;mannitol group with 5.5 mM D-glucose and 24.5 mM mannitol（MG）;all trans retinoic acid group with low concentrations（HG ＋ 10^-7 mol/LATRA,ATRA1）;all trans retinioc acid group with medium concentrations（HG ＋ 10^-6 mol/LATRA,ATRA2）;all trans retinioc acid group with high concentrations（HG ＋ 10^-5 mol/LATRA,ATRA3）;ethanol group with HG ＋ 10^-2 mol/L ethanol and Captopril group with HG ＋ 10^-5 mol/Lcaptopril.Cells in each group were cultured for 24 h,48 h and 72 h respectively.The concentration of FN and LN in the culture medium was detected by enzyme linked immunosorbent assay（ELISA）.Results High glucose could promote the expression of FN and LN in HK-2 cells（P 0.01）,which could be inhibited by ATRA（P 0.01）.Conclusion ATRA can inhibit the expression of FN and LN in HK-2 cells induced by high blood glucose.The inhibitory effect may be one of the potential measures to prevent from renal fibrillation with diabetic nephropathy.
出处
《临床医学工程》
2011年第7期992-994,共3页
Clinical Medicine & Engineering
