CAJ | 학술논문

目的探讨罗格列酮对高糖诱导的大鼠系膜细胞表达细胞间黏附分子1(ICAM-1)的影响及其可能机制. 方法采用正常糖(NG)、高糖(HG)及HG+不同浓度罗格列酮培养大鼠系膜细胞.以RT-PCR检测ICAM-1 mRNA的表达,采用ELISA检测培养细胞上清中ICAM-1蛋白的浓度.采用凝胶电泳迁移率改变法检测NF-κB的活性. 结果 HG组ICAM-1/GAPDH吸光度是NG组的2.9倍(P＜0.01).5 μmol/L及20 μmol/L罗格列酮均可显著抑制ICAM-1 mRNA的表达.HG刺激系膜细胞1 h可使NF-κB活性增强2.5倍(P＜0.01),高糖诱导的NF-κB的活化可被罗格列酮(20 μmol/L)所抑制(0.8±0.2 vs 2.5±0.3, P＜0.01). 结论罗格列酮可通过抑制NF-κB信号传导途径降低高糖诱导的系膜细胞ICAM-1的表达.
목적 탐토라격렬동대고당유도적대서계막세포표체세포간점부분자1(ICAM-1)적영향급기가능궤제. 방법 채용정상당(NG)、고당(HG)급HG+불동농도라격렬동배양대서계막세포.이RT-PCR검측ICAM-1 mRNA적표체,채용ELISA검측배양세포상청중ICAM-1단백적농도.채용응효전영천이솔개변법검측NF-κB적활성. 결과 HG조ICAM-1/GAPDH흡광도시NG조적2.9배(P＜0.01).5 μmol/L급20 μmol/L라격렬동균가현저억제ICAM-1 mRNA적표체.HG자격계막세포1 h가사NF-κB활성증강2.5배(P＜0.01),고당유도적NF-κB적활화가피라격렬동(20 μmol/L)소억제(0.8±0.2 vs 2.5±0.3, P＜0.01). 결론 라격렬동가통과억제NF-κB신호전도도경강저고당유도적계막세포ICAM-1적표체.
Objective To investigate the role of rosiglitazone in high glucose(HG)-induced intercellular adhesion molecule-1(ICAM-1) expression of rat mesangial cells.Methods The rat mesangial cells(MCs) were cultured in the medium with normal glucose(5.6 mmol/L,NG),high glucose(25 mmol/L,HG),HG+5 μmol/L rosiglitazone,HG+20 μmol/L rosiglitazone and HG+PDTC(αNF-κB inhibitor).ICAM-1 mRNA expression was measured by semi-quantitative RT-PCR assay.Activation of nuclear factor-κB(NF-κB) of rat mesangial cells was measured by electrophoretic mobility shift assay(EMSA).The levels of ICAM-1 in the supernatants were determined by enzyme-linked immunosorbant assay(ELISA.) Results RT-PCR results showed that high-glucose increased the ratio of PCR products of ICAM-1 over GAPDH to 2.9-fold,which was prevented by rosiglitazone(5 and 20 μmol/L) pre-treatment.The NF-κB binding activity was 2.5-fold higher in MCs exposed to HG as compared with NG(P<0.01).When the MCs were cultured in the presence of rosiglitazone(20 μmol/L) for 1 h,there was a highly significant reduction in NFκB binding activity(0.8±0.2 vs 2.5±0.3,P<0.01).Conclusions Rosiglitazone may inhibit high glucose-induced NF-κB activation and ICAM-1 expression in mesangial cells.These findings may provide an experimental evidence for further evaluating the possibly protective effect of rosiglitazone against diabetic nephropathy.