CAJ | 학술논문

目的：探讨罗格列酮对高糖诱导胰岛素抵抗（ IR）血管内皮细胞的保护作用及可能机制。方法将人脐静脉内皮细胞（ HUVECs）分为3组：正常对照组（ DMEM培养液，葡萄糖浓度为5.5 mmol·L-1）；高糖组（建立高糖诱导内皮细胞IR模型后，葡萄糖浓度为33 mmol·L-1的DMEM中培养24 h）；罗格列酮组（建立高糖诱导内皮细胞IR模型后，葡萄糖浓度为33 mmol·L-1的DMEM中加入10μmol·L-1罗格列酮干预24 h）。检测细胞存活率、细胞上清液一氧化氮（NO）和内皮素（ET-1）水平、线粒体膜电位和活性氧（ROS）变化，以及磷酸化I-κB 激酶（p-IKK）和 NF-κB 抑制蛋白（ IKBA）表达水平。结果与正常对照组比较，高糖组细胞存活率和NO水平下降，ET-1水平上升；线粒体膜电位下降， ROS含量升高；IKK磷酸化水平增加，IκBα蛋白表达下调（P〈0.01），罗格列酮可显著逆转上述变化（P〈0.05）。结论罗格列酮可改善高糖诱导血管内皮细胞IR，其机制与抑制ROS/ IKK 通路有关。
목적：탐토라격렬동대고당유도이도소저항（ IR）혈관내피세포적보호작용급가능궤제。방법장인제정맥내피세포（ HUVECs）분위3조：정상대조조（ DMEM배양액，포도당농도위5.5 mmol·L-1）；고당조（건립고당유도내피세포IR모형후，포도당농도위33 mmol·L-1적DMEM중배양24 h）；라격렬동조（건립고당유도내피세포IR모형후，포도당농도위33 mmol·L-1적DMEM중가입10μmol·L-1라격렬동간예24 h）。검측세포존활솔、세포상청액일양화담（NO）화내피소（ET-1）수평、선립체막전위화활성양（ROS）변화，이급린산화I-κB 격매（p-IKK）화 NF-κB 억제단백（ IKBA）표체수평。결과여정상대조조비교，고당조세포존활솔화NO수평하강，ET-1수평상승；선립체막전위하강， ROS함량승고；IKK린산화수평증가，IκBα단백표체하조（P〈0.01），라격렬동가현저역전상술변화（P〈0.05）。결론라격렬동가개선고당유도혈관내피세포IR，기궤제여억제ROS/ IKK 통로유관。
Objective To explore the protective effect of rosiglitazone on insulin resistance( IR)induced by high glucose in vascular endothelial cells and its possible mechanism. Methods Human umbilical vein endothelial cells( HUVECs) was divided into 3 groups:the normal control group cultivated in DEME medium with 5. 5 mmol·L-1 glucose;the high glucose group( HG)cultivated in DEME medium with 33 mmol · L-1 glucose for 24 h after the IR model was set up;the rosiglitazone group cultivated in DEME medium with 33 mmol·L-1 glucose and 10 μmol·L-1 of rosiglitazone for 24 h after the IR model was set up. The cell viability,nitric oxide(NO),endothelin-1(ET-1),mitochondrial membrane potential,reactive oxygen species ( ROS),p-IKK and IkBa protein levels were detected. Results Compared with the normal control,the cell viability,the level of NO and the mitochondrial membrane potential were decreased,levels of ET-1 and ROS increased,p-IKK expression was up-regulated,and IκBα expression was down-regulated in HG group(all P〈0. 01). Rosiglitazone reversed these changes in a time-dependent manner(P〈0. 05). Conclusion Rosiglitazone has the protective effect on insulin resistance induced by high glucose in vascular endothelial cells via inhibiting ROS/IKK signaling pathway.