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|

NLRP3/IL-1β信号通路在大鼠动脉粥样硬化中的炎症机制研究

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第2期
页码:
141-145
栏目:
基础研究
出版日期:
2018-02-15

文章信息/Info

Title:
Mechanism of NLRP3/Casepase-1/IL-1 beta signaling pathway in pathogenesis of atherosclerosis in rats
作者:
吴雨卉; 孙经武; 池天鹤
（滨州医学院烟台附属医院心血管内科，山东 烟台 264100）
Author(s):
WU Yu-hui;  SUN Jing-wu;  CHI Tian-he
(Department of Cardiology, Yantai Affiliated Hospital, Binzhou Medical University, Yantai 264100 Shandong, China)
关键词:
动脉粥样硬化; 泡沫细胞; 巨噬细胞; NLRP3; IL-1β
Keywords:
atherosclerosis;  foam cells;  macrophages;  NLRP3;  IL-1β
分类号:
R543.5
DOI:
-
文献标识码:
A
摘要:
目的 观察在Wistar大鼠动脉粥样硬化斑块形成过程中NLRP3及IL-1β的mRNA及蛋白质水平表达变化，了解NLRP3/IL-1β信号通路在动脉粥样硬化形成过程中发挥的作用。方法 采取维生素D3联合高脂饲料方法建立动脉粥样硬化模型。并分时间段取材，用实时荧光定量PCR及蛋白免疫印迹法检测NLRP3及IL-1β的mRNA及蛋白水平的表达变化。结果 在Wistar大鼠动脉粥样硬化形成过程中，随着时间的延长， NLRP3及IL-1β的RNA和(或)蛋白表达量则逐渐上升。结论 该研究提示NLRP3/IL-1β在大鼠动脉粥样硬化发展过程中明显增强，其作用和意义有待研究。
Abstract:
AIM To observe the expressions of mRNA and protein levels in the process of the formation of NLRP3 and IL-1 beta in atherosclerotic plaques of Wistar rats and to explore the role of the NLRP3/IL-1 beta signaling pathway in the formation process of atherosclerosis. METHODS The model of atherosclerosis was established by vitamin D3 combined with a high fat diet. The expressions of mRNA and protein in NLRP3 and IL-1 beta were detected by real-time fluorescent quantitative PCR and Western blotting. RESULTS In Wistar rats, the expressions of RNA and protein of NLRP3 and IL-1 beta increased gradually with the prolongation of time. CONCLUSION The results of this study suggest that NLRP3/IL-1 beta may play an important role in the development of atherosclerosis in rats.

参考文献/References

[1]Stein S,Lohmann C,Sch?fer N,et al.SIRT1 decreases Lox-1-mediated foam cell formation in atherogenesis[J].Eur Heart J,2010,31(18):2301-2309.

[2]Libby P,Okamoto Y,Rocha VZ,et al.Inflammation in Atherosclerosis:Transition From Theory to Practice[J].Circ J,2010,74(2):213-220.

[3]Wang L,Peng Q,Wang H,et al.NLRP3 inflammasome a novel link between lipoproteins and atherosclerosis[J].Arch Med Sci,2016,12(5):950-958.

[4]Duewell P,Kono H,Rayner KJ,et al.NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J].Nature,2010,464(7293):1357-1361.

[5]Wang L,Qu P,Zhao J,et al.NLRP3 and downstream cytokine expression elevated in the monocytes of patients with coronary artery disease[J].Arch Med Sci,2014,10(4):791-800.

[6]Menu P,Pellegrin M,Aubert JF,et al.Atherosclerosis in ApoE-deficient mice progresses independently of the NLRP3 inflammasome[J].Cell Death and Disease,2011,2(3):e137.

[7]da Motta NA,Kummerle AE,Marostica E,et al.Anti-atherogenic Effects of a New Thienylacylhydrazone Derivative,LASSBio-788,in Rats Fed a Hypercholesterolemic Diet[J].J Pharmacol Sci,2013,123(1):47-57.

[8]王园园,龙民慧,邹民吉,等.大鼠动脉粥样硬化动物模型的建立和评价［J］. 中国实验动物学报, 2008, 16(6):421-423.

[9]Lee HM, Kim JJ, Kim HJ, et al. Upregulated NLRP3 inflammasome activation in patients with type 2 diabetes[J].Diabetes,2013,62(1):194-204.

[10]Mao Z,Liu C,Ji S,et al.The NLRP3 Inflammasome is Involved in the Pathogenesis of Parkinson’s Disease in Rats[J].Neurochem Res,2017,42(4):1104-1115.

[11]Tran H,Jacqueline T,Hira S,et al.Role of interleukin-1 inhibitors in the management of gout[J].Pharmacotherapy,2013,33(7):744-53.

[12]Lin J,Shou X,Mao X,et al.Oxidized low density lipoprotein induced caspase-1 mediated pyroptotic cell death in macrophages:implication in lesion instability?[J].PLoS ONE,2013,8(4):e62148.

[13]Jiang Y,Wang M,Huang K,et al.Oxidized low-density lipoprotein induces secretion of interleukin-1beta by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation[J].Biochem Biophys Res Commun,2012,425(2):121-126.

[14]Liu W,Yin Y,Zhou Z,et al.OxLDL-induced IL-1 beta secretion promoting foam cells formation was mainly via CD36 mediated ROS production leading to NLRP3 inflammasome activation[J].Inflamm Res,2014,63(1):33-43.

[15]Martinon F,Pétrilli V,Mayor A,et al.Gout-associated uric acid crystals activate the NALP3 inflammasom[J].Natrue,2006,440(7081):237-241.

[16]Carta S,Tassi S,Semino C,et al.Histone deacetylase inhibitors prevent exocytosis of interleukin-1 containing secretory lysosomes:role of microtubules[J].Blood,2006,10(8):1618-1626.

[17]Franz-Wachtel M,Eisler SA,Krug K,et al.Global detection of protein kinase D-dependent phosphorylation events in nocodazole-treated human cells[J].Mol Cell Proteomics,2012,11(5):160-170.

[18]Misawa T,Takahama M,Kozaki T,et al.Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome[J].Nat Immunol,2013,14(5):454-460.

备注/Memo

备注/Memo:
收稿日期：2017-03-27.通讯作者：孙经武，主任医师，主要从事冠心病发病机制的研究 Email：bysjw@163.com 作者简介：吴雨卉，硕士生 Email：wuyuhui0707@163.com
更新日期/Last Update: 1900-01-01