Liraglutide prevents high glucose-induced adhesion of endothelial cells to monocyte by targeting IKK/NF-κB
10.3760/cma.j.issn.1008-1372.2019.06.008
- VernacularTitle:利拉鲁肽对高糖诱导的人脐静脉内皮细胞与单核细胞黏附的影响及作用机制
- Author:
Hu LI
1
;
Qing SHU
;
Xian YANG
;
Xuemei LUO
;
Simin YAN
Author Information
1. 南京大学医学院附属鼓楼医院心脏科 210008
- Keywords:
Liraglutide;
Endothelial cells;
Monocytes;
Cell adhesion;
In vitro
- From:
Journal of Chinese Physician
2019;21(6):830-834,839
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibition effect of liraglutide (lira) on high glucose-induced adhesion of endothelial cells to monocyte.Methods Human umbilical vascular endothelial cells (HUVECs) induced by high glucose (20 mmol/L) were incubated with different concentrations of liraglutide (0,0.3,3,30 nmol/L) for different time.THP-1 cells were pre-labeled with Calcein-AM and then incubated with HUVECs for 1 h,M199 medium were used for washing the nonadherent cells for 3 times,and the adhesion of HUVECs to THP-1 cells were measured by Fluorence microplate reader;real-time polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA) were employed to detect the mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1),respectively.Western blot was used to measure the content of IκBα,p-IκBα and the distribution of p65 in plasma and nuclear.GST-IκBα was introduced as substrate to test the activity of IκB-kinase (IKK).Results The adhesion of HUVECs to THP-1 (P ＜ 0.01),the mRNA and protein expression of VCAM-1 and ICAM-1 (P ＜ 0.05,P ＜ 0.01),the phosphorylation of κBα (P ＜ 0.05,P ＜ 0.01),the translocation of p65 subunit from plasma to nuclear and the activity of IKK (P ＜ 0.01) in HUVECs were all elevated by stimulation with 20 mmol/L glucose,and the content of IκBα was decreased accordingly (P ＜0.01).Pre-incubation with lira could reverse the above effect of high concentration of glucose.Conclusions Lira could reduce VCAM-1 and ICAM-1 expression through IKK/NF-κB pathways in 20 mmol/L glucose-induced HUVECs,which finally suppress THP-1-HUVECs adhesion.
