我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

脂联素抑制炎症小体NLRP3表达减轻高糖高脂诱导内皮细胞损伤

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第6期
页码:
634-637
栏目:
基础研究
出版日期:
2016-07-05

文章信息/Info

Title:
Adiponectin decreases endothelial cell injury by inhibiting expression of NLRP3 inflammasome
作者:
张静隆; 朱 迪; 王贺林; 辛 超; 李 燕; 刘 毅; 陶 凌
(第四军医大学西京医院心血管内科，陕西 西安 710032）
Author(s):
ZHANG Jing-long;  ZHU Di;  WANG He-lin;  XIN Chao;  LI Yan;  LIU Yi;  TAO Ling
(Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
脂联素; 人脐静脉内皮细胞; 高糖高脂; 炎症小体NLRP3
Keywords:
adiponectin;  HUVEC;  high glucose/high fat;  NLRP3 inflammasome
分类号:
R738.1
DOI:
-
文献标识码:
A
摘要:
目的 研究脂联素（APN）是否通过抑制炎症小体NLRP3表达减轻高糖高脂所致的内皮细胞损伤。方法 将培养的人脐静脉内皮细胞（human umbilical vein endothelial cells，HUVECs）分为6组：对照组、高糖高脂组、对照+ NLRP3 siRNA组，高糖高脂组+NLRP3 siRNA组，对照+APN组，高糖高脂+APN组。培养48 h后检测细胞存活率、凋亡率、炎症小体NLRP3表达水平。结果 与对照组相比，高糖高脂组细胞存活率显著下降，细胞凋亡显著升高，炎症小体NLRP3表达水平显著升高（均P<0.05）；炎症小体NLRP3 siRNA可有效的抑制炎症小体NLRP3的表达，改善高糖高脂引起的内皮细胞损伤（均P<0.05）；APN能抑制高糖高脂引起的炎症小体NLRP3表达增多，进而减轻高糖高脂引起的内皮损伤（均P<0.05）。结论 炎症小体NLRP3表达增多是高糖高脂诱导人脐静脉内皮细胞凋亡的内在机制，而脂联素可以通过抑制炎症小体NLRP3的过度表达发挥内皮保护作用。伤，降低心肌炎症反应。
Abstract:
AIM To investigate whether adiponectin (APN) exerts endothelial protection in response to high glucose/high-fat damage through inhibiting expression of NLRP3 inflammasome. METHODSCultured human umbilical vein endothelial cells (HUVECs) were randomly divided into control group (5 mmol/L glucose, 20 mmol/L mannitol, 48h incubation), high glucose/high-fat group (25 mmol/L glucose, 500μmol/L sodium palmitate, 48 h incubation), control+siRNA group (5 mmol/L glucose, 20 mmol/L mannitol and NLRP3 specific siRNA, 48 h incubation), high glucose/high fat+siRNA group (25 mmol/L glucose, 500 μmol/L sodium palmitate and NLRP3 specific siRNA, 48 h incubation), control+APN group (5 mmol/L glucose, 20 mmol/L mannitol and 2 μg/ml APN, 48 h incubation) and high glucose/high-fat+APN group (25 mmol/L glucose, 500 μmol/L sodium palmitate and 2 μg/ml APN, 48 h incubation). Cells from these groups were harvested for evaluation of cell viability, apoptosis rate and NLRP3 inflammasome expression. RESULTSCompared with control group, cell viability decreased, and NLRP3 inflammasome expression and apoptosis rate increased in high glucose/high-fat group (all P<0.05). These changes were all reversed by NLRP3 specific siRNA and APN (all P<0.05). CONCLUSIONHigh glucose/high fat leads to increased expression of NLRP3 inflammasome, thereby causing cell injury in HUVECs. APN can protect HUVECs by inhibiting expression of the NLRP3 inflammasome.

参考文献/References

[1]Yang SH,Dou KF,Song WJ. Prevalence of diabetes among men and women in china[J].N Engl J Med,2010,362(25):2425-2426.
[2]Calles-Escandon J,Cipolla M.Diabetes and endothelial dysfunction:a clinical perspective[J].Endocr Rev,2001,22(1):36-52.
[3]Shimabukuro M,Higa N,Asahi T,et al.Hypoadiponectinemia is closely linked to endothelial dysfunction in man[J].J Clin Endocrinol Metab,2003,88(7):3236-3240.
[4]Tan KC,Xu A,Chow WS,et al.Hypoadiponectinemia is associated with impaired endothelium-dependent vasodilation[J].J Clin Endocrinol Metab,2004,89(2):765-769.
[5]Maruyoshi H,Kojima S,Otsuka F,et al.Hypoadiponectinemia is associated with coronary artery spasm in men[J].Circ J,2005,69(9):1154-1156.
[6]Martinon F,Burns K,Tschopp J.The inflammasome:a molecular platform triggering activation of inflammatory caspases[J].Mol Cell,2002,10(2):417-426.
[7]Stutz A,Golenbock DT,Latz E,et al.Inflammasomes:too big to miss[J].J Clin Invest,2009,119(12):3502-3511.
[8]Menu P,Vince JE.The NLRP3 inflammasome in health and disease:the good, the bad and the ugly[J].Clin Exp Immunol,2011,166(1):1-15.
[9]Liu Y,Lian K,Zhang L,et al.TXNIP mediates NLRP3 inflammasome activation in cardiac microvascular endothelial cells as a novel mechanism in myocardial ischemia/reperfusion injury[J].Basic Res Cardiol,2014,109(5):415-419.
[10]Yi W,Sun Y,Gao E,et al.Reduced cardioprotective action of adiponectin in high-fat diet-induced type II diabetic mice and its underlying mechanisms[J].Antioxid Redox Signal, 2011, 15(7):1779-1788.
[11]Colavitti R, Pani G, Bedogni B,et al.Reactive oxygen species as downstream mediators of angiogenic signaling by vascular endothelial growth factor receptor-2/KDR[J].J Biol Chem,2002,277(5):3101-3108.
[12]Ning S,Bednarski M,Oronsky B,et al.Novel nitric oxide generating compound glycidyl nitrate enhances the therapeutic efficacy of chemotherapy and radiotherapy[J].Biochem Biophys Res Commun,2014,447(3):537-542.
[13]Kim JE,Song SE,Kim YW,et al.Adiponectin inhibits palmitate-induced apoptosis through suppression of reactive oxygen species in endothelial cells:involvement of cAMP/protein kinase A and AMP-activated protein kinase[J].J Endocrinol,2010,207(1):35-44.
[14]Creager MA,Lüscher TF,Cosentino F,et al.Diabetes and vascular disease:pathophysiology, clinical consequences,and medical therapy:Part I.[J].Circulation,2003,108(12):1527-1532.
[15]Ehsan M,Singh KK,Lovren F,et al.Adiponectin limits monocytic microparticle-induced endothelial activation by modulation of the AMPK, Akt and NFκB signaling pathways[J].Atherosclerosis,2015,245(1):1-11.

备注/Memo

备注/Memo:
收稿日期：2015-11-24
基金项目：国家杰出青年基金项目资助（81225001）；新世纪优秀人才支持计划项目资助（NCET-11-0870）
通讯作者：陶凌，教授，主要从事缺血性心肌损伤研究Email:lingtao2006@gmail.com
共同通讯作者：刘毅，主治医师，主要从事缺血性心肌损伤研究Email:liuyimeishan@hotmail.com
作者简介：张静隆，硕士生Email：zhangjinglong2013@126.com
更新日期/Last Update: 2016-07-10