Effects and mechanism of glucagon-like peptid-1 on atherosclerosis

AIM To investigate the effects and mechanism of glucagon-like peptid-1 (GLP-1) against human umbilical vein endothelial cells (HUVECs) injured by oxidized low-density lipoprotein (ox-LDL). METHODSCultured HUVECs were divided into control group (without treatment) and GLP-1 pretreatment groups (pretreated with 0, 2.5, 5, 10 nmol/L GLP-1 for 24 h and then added to 100 μg/ml ox-LDL for 24 h). Effects of GLP-1 on the activity of HUVECs induced by oxidized low-density lipoprotein (ox-LDL) were detected by MTT assay and the effects of GLP-1 on the adhesion of monocytes with HUVECs induced by ox-LDL were studied. Secretions of E-selectin, intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule (VCAM-1) by HUVECs were measured by ELISA and mRNA levels of ICAM-1, VCAM-1 and E-selectin of HUVECs were analyzed by real time RT-PCR. RESULTSMTT results indicated that GLP-1 (2.5, 5, 10 μmol/L) could inhibit HUVECs injury induced by ox-LDL in a concentration-dependent manner (P<0.05). Adhesion of monocytes with HUVECs induced by ox-LDL was inhibited by GLP-1 in a concentration-dependent manner (P<0.05). Levels of ICAM-1, VCAM-1 and E-selectin in GLP-1 groups were significantly decreased compared with those in ox-LDL-simulated group (P<0.05). mRNA expressions of ICAM-1, VCAM-1 and E-selectin in GLP-1 groups were also significantly downregulated compared with those in ox-LDL-simulated group (P<0.05). CONCLUSIONGLP-1 can prevent atherosclerotic lesion. The mechanisms may be that GLP-1 can defend against oxidation damage to HUVECs, inhibit adhesion of monocytes to HUVECs and reduce the secretion and expression of adhesion molecules including ICAM-1, VCAM-1 and E-selectin.