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|

NF-κB在TNF-α致人脐静脉内皮细胞凋亡中的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第2期
页码:
152-154
栏目:
基础研究
出版日期:
2006-03-01

文章信息/Info

Title:
Role of NF-κB in endothelial cell apoptosis induced by TNF-α
作者:
郭瑞威杨丽霞石燕昆齐峰郭传明
成都军区昆明总医院心血管内科,云南 昆明 650032
Author(s):
GUO Rui-wei YANG Li-xia SHI Yan-kun QI Feng GUO Chuan-ming
Department of Cardiology, Kunming General Hospital, Chengdu Military Area Command, Kunming,Yunnan 650032, China
关键词:
核转录因子-κB内皮细胞肿瘤坏死因子-α凋亡
Keywords:
nulear factor-κBendothelial cellstumor necrosis factor-αapoptosis
分类号:
R329.28
DOI:
-
文献标识码:
A
摘要:
目的 研究核转录因子-κB (nuclear factor-κB,NF-κB)在TNF-α诱导培养的人脐静脉内皮细胞凋亡过程中的作用。方法体外培养人脐静脉内皮细胞,并用10 ng/ml的TNF-α进行诱导,不同时间段观察NF-κB活性、NF-κB抑制物IκBα表达以及细胞凋亡的情况,EMSA测定NF-κB活性,Western-blot检测IκBα的表达情况;Tunel法检测细胞凋亡;并用NF-κB 的抑制剂PDTC预处理细胞后来观察TNF-α诱导细胞凋亡的情况。结果TNF-α以时间依赖性诱导人脐静脉内皮细胞凋亡,NF-κB的活性在处理后10 min开始增强,2 h后恢复正常,IκBα的表达在10 min开始下降,2 h恢复正常;PDTC能抑制TNF-α诱导的凋亡。结论TNF-α在诱导体外培养的人脐静脉内皮细胞时,IκBα降解,NF-κB激活,从而引起细胞的凋亡。
Abstract:
AIM To study the role of nulear factor-κB (NF-κB) in endothelial cell apoptosis induced by TNFα. METHODS The cultured endothelial cells were treated with 10 ng/ml TNF-α in absence and presence of PDTC (an inhibitor of NF-κB), the activity of NF-κB was measured by e1lectrophoretic mobility shift assay (EMSA), the expression of IκBα was analyzed by western blotting and apoptosis of cells was evaluated by TUNEL. RESULTS TNF-α induced apoptosis of endothelial cells in a timedependant manner. The activity of NF-κB began to increase and the expression of IκBα began to decrease at 10 min after treatment with TNF-α. PDTC inhibited the apoptosis induced by TNF-α. CONCLUSION TNF-α activates NF-κB through phosphorylation of IκBα and thus induces apoptosis of endothelial cells.

参考文献/References

[1]Monaco C,Paleolog E.Nuclear factor κB:a potential therapeutic target in atherosclerosis and thrombosis[J]. Cardiovasc Res,2004,61:671-682.

[2] Madan B, Singh I, Kumar A,et al. Xanthones as inhibitors of microsomal lipid peroxidation and TNFalpha induced ICAM1 expression on human umbilical vein endothelial cells (HUVECs) [J]. Bioorg Med Chem, 2002,10(11): 3431-3436.

[3] Cuschleri J,Gourlay D,Garcia I,et al.Endotoxininduced endothelial cell proinflammatory phenotypic differentiation requires stress fiber polymerization[J]. Shock,2003,19(5): 433-439.

[4] 王斌,赵连友,郑强荪,等. 单核细胞趋化蛋白1对高血压心肌纤维化的作用及其与转化生长因子β的关系[J].心脏杂志,2004,16(5):417-420.

[5] Zandi E,Chen Y,Karm M.Direct phosphorylation of IκB by IKKα and IKK β:discrimination between free and NFκB bound substrate[J]. Science,1998,281:1360-1363.

[6] 潘晓明,吴宗贵,黄佐,等. TNFa水平对急性心肌梗死预后的影响[J].心脏杂志,2004,16(1):39-40.

[7] Garg AK,Aggarwal BB.Reactive oxygen intermediates in TNF signaling[J]. Mol Immunol,2002,39:509-517.

[8] Luschen S,Scherer G,Ussat S,et al. Inhibitor of p38 mitogenactivated protein kinase reduces TNFinduced activation of NFκB,elicits caspase activity,and enhances cytotoxicity[J]. Exp Cell Res,2004,293:196-206.

备注/Memo

备注/Memo:
收稿日期:2005-09-16.基金项目:云南省科委自然科学基金项目资助(No.2001C0070W) 通讯作者:杨丽霞,主任医师,主要从事心力衰竭基础与临床的研究 作者简介:郭瑞威,硕士生 Tel:(0871)4074571 Email:grw771210@163.com
更新日期/Last Update: