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|本期目录/Table of Contents|

核因子κB在心肌缺血/再灌注损伤中的作用

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2009年第2期
页码:
271
栏目:
综述
出版日期:
2009-03-30

文章信息/Info

Title:
-
作者:
余伟 综述王伟 审校
汕头大学医学院第一附属医院心血管内科,广东 汕头 515041
Author(s):
-
关键词:
核因子κB心肌缺血/再灌注心肌炎症细胞凋亡氧化应激
Keywords:
-
分类号:
R541.4
DOI:
-
文献标识码:
A
摘要:
核因子κB(NF-κB)是一种多效转录因子,在心肌缺血/再灌注损伤的病理生理过程中起着关键作用,参与了对心肌炎症反应、细胞凋亡和氧化应激过程的调控。
Abstract:
-

参考文献/References

[1] Brown M, McGuinness M, Wright T, et al. Cardiac-specific blockade of NF-κB in cardiac pathophysiology: differences between acute and chronic stimuli in vivo[J]. Am J Physiol Heart Circ Physiol, 2005, 289(1):H466-H476.

[2] Zhang M, Xu YJ, Saini HK, et al. Pentoxifylline attenuates cardiac dysfunction and reduces TNF-α level in ischemic-reperfused heart[J]. Am J Physiol Heart Circ Physiol, 2005, 289(2):H832-H839.

[3] Yeh CH, Chen TP, Wu YC, et al. Inhibition of NFκB activation with Curcumin attenuates plasma inflammatory cytokines surge and cardiomyocytic apoptosis following cardiac ischemia-reperfusion[J]. J Surg Res, 2005, 125(1):109-116.

[4] Liakopoulos OJ, Schmitto JD, Kazmaier F, et al. Cardiopulmonary and systemic effects of methylprednisolone in patients undergoing cardiac surgery[J]. Ann Thorac Surg, 2007, 84(1):110-118.

[5] Gu Q, Yang XP, Bonde P, et al. Inhibition of TNF-alpha reduces myocardial injury and proinflammatory pathways following ischemia-reperfusion in the dog[J]. J Cardiovasc Pharmacol, 2006, 48(6):320-328.

[6] Shimamoto A, Chong AJ, Yada M, et al. Inhibition of Toll-like receptor 4 with Eritoran attenuates myocardial ischemia-reperfusion injury[J]. Circulation, 2006, 114(1 Suppl):I270-I274.

[7] Stansfield WE, Moss NC, Willis MS, et al. Proteasome inhibition attenuates infarct size and preserves cardiac function in a murine model of myocardial ischemia-reperfusion injury[J]. Ann Thorac Surg, 2007, 84(1):120-125.

[8] Frantz S, Tillmanns J, Kuhlencordt PJ, et al. Tissue-specific effects of the nuclear factor kappaB subunit p50 on myocardial ischemia-reperfusion injury[J]. Am J Pathol, 2007, 171(2):507-512.

[9] Choi H, Kim SH, Chun YS, et al. In vivo hyperoxic preconditioning prevents myocardial infarction by expressing Bcl-2[J]. Exp Biol Med, 2006, 231(4):463-472.

[10]Kin H, Wang NP, Halkos ME, et al. Neutrophil depletion reduces myocardial apoptosis and attenuates NFkappaB activation/TNFalpha release after ischemia and reperfusion[J]. J Surg Res, 2006, 135(1):170-178.

[11]郭瑞威,杨丽霞,石燕昆,等. NF-κB在TNF-α致人脐静脉内皮细胞凋亡中的作用[J]. 心脏杂志, 2006, 18(2):152-154.

[12]杨晓云,周宁,王琳,等. 辛伐他汀对NF-κB-DNA结合活性和表达的影响[J]. 心脏杂志, 2006, 14(4):369-372.

[13]Rui T, Kvietys PR. NFkappaB and AP-1 differentially contribute to the induction of MnSOD and eNOS during the development of oxidant tolerance[J]. FASEB J, 2005, 19(13):1908-1910.

[14]刘颖,吴伟康,陈晨,等. 核因子-κB在四逆汤预处理诱导大鼠心肌延迟预适应中的作用[J]. 中国中药杂志, 2005, 30(6):453-456.

[15]Li Q, Guo Y, Tan W, et al. Cardioprotection afforded by inducible nitric oxide synthase gene therapy is mediated by cyclooxygenase-2 via a nuclear factor-κB dependent pathway[J]. Circulation, 2007, 116(14):1577-1584.

备注/Memo

备注/Memo:
收稿日期:2008-1-11.基金项目:广东省自然科学基金重点项目资助(05008363) 通讯作者:王伟,主任医师,主要从事冠心病的诊治研究Email:stwangwei@126.com 作者简介:余伟,硕士生Email:yuwei10610048@126.com
更新日期/Last Update: 2009-04-16