期刊
DIABETES METABOLIC SYNDROME AND OBESITY-TARGETS AND THERAPY
卷 12, 期 -, 页码 1931-1942出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DMSO.S222053
关键词
NLRP3 inflammasome; diabetes; atherosclerosis; inflammation
资金
- Natural Science Funds of Shaanxi Province [2016JM8059]
Background: NLRP3 inflammasome can be activated by high glucose and links inflammation and metabolic disease. This study aimed to investigate the role of NLRP3 inflammasome in hyperglycemia-induced endothelial inflammation and diabetic atherosclerosis. Methods: NLRP3 levels in peripheral blood mononuclear cell (PBMC) and plasma IL-1 beta level were measured in diabetes patients. The activation of NLPR3 was detected in diabetic ApoE-/- mice and human umbilical vein endothelial cells (HUVECs). Results: Compared with healthy controls, NLRP3 expression levels in PBMC and plasma IL-1 beta level were significantly higher in diabetes patients but considerably decreased after lifestyle interventions and medicine. Moreover, carotid atherosclerosis was significantly related to plasma IL-1 beta level in diabetes patients. In diabetic atherosclerosis mouse model, NLRP3 knockdown suppressed NLRP3 inflammasome activation, inhibited the expression of adhesion molecules ICAM-1 and VCAM-1 in intima, reduced atherosclerosis and stabilized atherosclerotic plaque. In vitro, the expression of NLRP3 inflammasome components and the secretion of IL-1 beta were augmented by high glucose in HUVECs. Moreover, either high glucose or IL-1 beta promoted the expression of adhesion molecules, which were suppressed by NLRP3 knockdown or IL-1 beta receptor antagonist. Conclusion: These findings provide novel insights into pathological mechanisms of diabetic atherosclerosis and have potential therapeutic implications for cardiovascular complications in diabetes.
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