Effect of Rosiglitazone on Insulin Resistance and ROS . IKK Signaling Pathway in Vascular Endothelial Cells / 医药导报

ABSTRACT

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 groupsthe 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.