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Pages: 257-259+264
Year: Issue:  3
Journal: Acta Aacademiae Medical Qingdao Universitatis

Keyword:  AVE3085endothelial cellsnitric oxide synthasegene expressionreactive oxygen speciesapoptosis;
Abstract: Objective To explore the protection effect of AVE3085 on ADMA-induced human coronary artery endothelial cells(HCAEC)dysfunction. Methods The primary culture of HCAECs was divided into four groups-control,ADMA,ADMA+AVE3085and ADMA+DMSO-and cultured for 24 hin culture containing the corresponding medicine,and then the expression of eNOS-mRNA in the cells was detected using RT-PCR technique,protein expressions of eNOS and p-eNOSser1177 were determined using Western-blot,and the release of NO and the formation of ROS were measured employing fluorescence probe,the apoptosis was tested using a flow cytometry. Results Compared with the control group,the expression of eNOS in the AMDA group markedly down-regulated,the release of NO declined,the formation of ROS increased,and the number of apoptotic cells greatly increased,the difference being significant(F=361.55-1 041.17,q=23.55-80.50,P<0.01).Compared with the ADMA group,the expression of eNOS in the ADMA+AVE3085group notably elevated,the release of NO increased,the formation of ROS declined,and the number of apoptotic cells decreased,the difference being significant(q=21.91-36.83,P<0.01).Conclusion ADMA has a damage effect on human coronary artery endothelial cells.AVE3085 plays a protective effect on the cells through up-regulating expression of eNOS,promoting release of NO,suppressing formation of ROS and apoptosis.
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