Study on Inhibitory Effects of Minocycline on HUVECs-lymphomonocyte Adhesion and Its Mechanism
10.6039/j.issn.1001-0408.2015.31.20
- VernacularTitle:米诺环素对人脐静脉内皮细胞-单核细胞黏附的抑制作用及其机制研究
- Author:
Li CHEN
;
Naijun ZHU
;
Yuan YUAN
- Publication Type:Journal Article
- Keywords:
Minocycline;
Endothelial cells;
Monocyte;
Adhesion;
Adhesion molecule;
NF-κB p65
- From:
China Pharmacy
2015;26(31):4381-4384
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the inhibitory effects of minocycline (MC) on TNF-α induced monocyte-endothelial adhe-sion and the relative mechanism. METHODS:Primary human umbilical vein endothelial cells (HUVECs) were isolated from hu-man umbilical veins with enzyme digestion. HUVECs were divided into blank control group,model group,MC low-dose,medi-um-dose and high-dose groups(1,10,100 μmol/L). After treated for 2 h,10 ng/ml TNF-α was employed to stimulate monocytes THP-1 adhesion with HUVECs except for blank control group,in order to induce monocyte-endothelial adhesion model. The num-ber of adherent cell was observed by fluorescence microscope,and fluorescence intensity was detected by microplate reader. Flow cytometry was adopted to detect the expression of intercellular adhesion molecule (ICAM)-1. The expressions of NF-κB p65 pro-tein in cell nucleus and cytoplasm were detected by Western blot. RESULTS:Compared with blank control group,the number and fluorescence intensity of adherent cell,the expression of ICAM-1 and the protein expression of NF-κB p65 in nucleus were all in-creased in model group,while the protein expression of NF-κB p65 in cytoplasm was weakened,with statistical significance(P<0.01). Compared with model group,the number and fluorescence intensity of adherent cell,the expression of ICAM-1 were all de-creased in MC low-dose,medium-dose and high-dose groups;the protein expression of NF-κB p65 in nucleus was weakened in MC medium-dose and high-dose groups,while the protein expression of NF-κB p65 in cytoplasm was heightened,with statistical significance (P<0.01 or P<0.05). CONCLUSIONS:MC can inhibit TNF-α induced monocyte-endothelial adhesion by a likely mechanism of reducing the expression of ICAM-1 in HUVECs and inhibiting the expression of NF-κB p65 protein.
