摘要
Abstract
Objective To investigate the effect of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in human umbilical vein endothelial cells (HUVECs) on lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression.
<br> Methods In vitro cultured HUVECs were taken intervention by ifnal concentration of 0, 10, 50, 100 ng/ml of recombinant human TWEAK (rhTWEAK) for 24 h, and fluorescence quantitative polymerase chain reaction (PCR) technology was used to detect the relative expression of TWEAK group LOX-1 mRNA detection of different doses. Meanwhile, after HUVECs cells were intervened with by previously having added ifnal concentration 0.2, 1, 10 μmol/L atorvastatin for 24 h, then coupled with a concentration of 100 ng/ml TWEAK incubated for 24 h, followed by PCR to detect the relative expression of LOX-1 mRNA; and enzyme-linked immunosorbent assay (ELISA) method was used to detect the cell supernatant LOX-1 protein expression. At the same time, morphological changes in each group were observed by lfuorescence microscopy.
<br> Results LOX-1 mRNA 2-△△Ct values of final concentration of 0, 10, 50, 100 ng/ml TWEAK intervention group and the relative expression of LOX-1 protein of the supernatant of each group were compared with the control group, which had statistically significant difference (P<0.001). TWEAK increased with increasing concentration of LOX-1 expression levels in different dose groups, which had significant difference (P<0.001); final concentration 0.2, 1, 10 μmol/L atorvastatin intervention group after the intervention significantly inhibited the expression of LOX-1 mRNA and protein compared with 100 ng/ml TWEAK group, which had significant difference (P<0.001); and there were signiifcant differences of inter-group comparison of different concentrations of atorvastatin group (P<0.001).
<br> Conclusion TWEAK can induce increased expression of human umbilical vein endothelial cells LOX-1, which may correlate with atherosclerosis. Atorvastatin could inhibit LOX-1 expression, which may be one of the mechanisms to play the anti-inlfammatory and anti-atherosclerosis role.关键词
动脉粥样硬化/肿瘤坏死因子样凋亡微弱诱导剂/血凝素样氧化低密度脂蛋白受体-1/阿托伐他汀/内皮细胞Key words
Tumor necrosis factor-like weak inducer of apoptosis/Lectin-like oxidized low-density lipoprotein receptor -1/Atorvastatin/Endothelial cell
