中国动脉硬化杂志2018，Vol.26Issue(3)：227-231,236,6.
白细胞介素37对Toll样受体4激活人冠状动脉内皮细胞核因子κB和细胞间黏附分子1表达的影响
Effect of interleukin-37 on the expressions of nuclear factor-κB and intercellular adhesion molecule-1 activated by Toll-like receptor-4 in human coronary artery endothelial cells
摘要
Abstract
Aim To explore the effect of anti-inflammation cytokine interleukin-37 (IL-37) on the expressions of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) activated by Toll-like receptor-4 (TLR4) in human coronary artery endothelial cells (HCAECs) and its mechanism.Methods After 3-5 generations of HCAECs culture,the experiment was carried out and divided into 3 groups:the control group,the IL-37 interference group and the IL-37 overexpression group.The IL-37 interference sequence was added into the IL-37 interference group and the IL-37 DNA overexpressed plasmid was added to the IL-37 overexpression group by liposome transfection.After incubation of 24 hours,the gene transfection efficiency was detected by real-time fluorescence quantitative PCR to determine the success of transfection.Each group was given TLR4 activator lipopolysaccharide (200 μg/L) for intervention.Western blot was used to detect the expression of ICAM-1 protein after intervention of 24 hours and the expressions of phosphorylated NF-κB protein at 30,60,120 minutes after intervention.Results The expression of ICAM-1 protein increased after TLR4 activation in the control group.Compared with the control group,the ICAM-1 protein increased significantly after TLR4 activation in the IL-37 interference group (P＜0.05),but did not increase in the IL-37 overexpression group (P＞0.05).Compared with the control group,the expression of NF-κB protein was significantly increased at 30,60 and 120 minutes after TLR4 activation in the IL-37 interference group (P＜0.05),but the expression of phosphorylated NF-κB protein was not significantly elevated in the IL-37 overexpression group (P＞0.05).Conclusion IL-37 can inhibit the increase of inflammatory factor ICAM-1 by TLR4 activation in HCAECs,and its mechanism may be through the inhibition of the degree of NF-κB phosphorylation.The anti-inflammatory effect of IL-37 can prevent atherosclerosis.关键词
白细胞介素37/人冠状动脉内皮细胞/Toll样受体4/核因子κB/细胞间黏附分子1/动脉粥样硬化Key words
Interleukin-37/Human coronary artery endothelial cell/Toll-like receptor-4/Nuclear factor-κB/Intercellular adhesion molecule-1/Atherosclerosis分类
医药卫生引用本文复制引用
谢康琪,谢燕丹,林玲,李吉林..白细胞介素37对Toll样受体4激活人冠状动脉内皮细胞核因子κB和细胞间黏附分子1表达的影响[J].中国动脉硬化杂志,2018,26(3):227-231,236,6.基金项目
国家自然科学基金(81672640) （81672640）
广东省自然科学基金(2015A030313441) （2015A030313441）
