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|本期目录/Table of Contents|

普罗布考对糖基化终末产物引发心脏微血管内皮功能紊乱的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第3期
页码:
324-327
栏目:
基础研究
出版日期:
2012-06-25

文章信息/Info

Title:
Effect of probucol on advanced glycosylation end product-induced dysfunction in cardiac microvascular endothelial cells
作者:
成永霞1刘贵波2于建渤1郭素芬1颜 彬1 李志强1杨向红3
(牡丹江医学院:1.病理学教研室,2.解剖学教研室,黑龙江 牡丹江157011;3.中国医科大学附属盛京医院病理科,沈阳 100011)
Author(s):
CHENG Yong-xia1 LIU Gui-bo2 YU Jian-bo1 GUO Su-fen1 YAN Bin1 Li Zhi-qiang1 YANG Xiang-hong3
(1.Department of Pathology, 2.Department of Anatomy, Mudanjiang Medical College, Mudanjiang 157011, Heilongjiang, China; 3.Department of Pathology, Affiliated Shengjing Hospital, China Medical University, Shenyang 100011, China)
关键词:
心脏微血管内皮细胞糖基化终末产物普罗布考诱导型一氧化氮合酶
Keywords:
cardiac microvascular endothelial cells advanced glycosylation end products probucol iNOS
分类号:
R36;R972
DOI:
-
文献标识码:
A
摘要:
目的:观察普罗布考(probucol)对糖基化终末产物(AGEs)作用后的心脏微血管内皮细胞iNOS表达的影响。方法: 原代培养心脏微血管内皮细胞,AGEs(100 mg/L)体外模拟高糖环境,在probucol(5 μmol/L,10 μmol/L,20 μmol/L) 作用后,检测ROS、NO和iNOS变化情况。结果: 与AGEs组比较,probucol组中ROS蛋白表达降低,NO生成增加,而 iNOS蛋白表达降低,且显示有浓度依赖性。结论: probucol可能通过对抗氧化应激的途径,缓解AGEs引发的心脏微血管内皮功能障碍。
Abstract:
AIM:To observe the effect of probucol on the iNOS expression induced by advanced glycosylation end products (AGEs) in cardiac microvascular endothelial cells. METHODS: Primary cardiac microvascular endothelial cells were cultured in vitro. After treatment with AGEs (100 mg/L) and probucol (5 μmol/L, 10 μmol/L, 20 μmol/L), NO, iNOS and ROS protein expressions in all groups were detected and compared between groups. RESULTS: Compared with AGEs group, NO and iNOS protein expression increased and ROS protein expression decreased in groups treated with probucol. CONCLUSION: Probucol is able to partially recover AGE-induced dysfunction in cardiac microvascular endothelial cells.

参考文献/References

[1]Brownlee M.Biochemistry and molecular cell biology of diabetic complications[J].Nature,2001,414(6865):813-820.

[2]Hamilton SJ,Chew GT,Watts GF.Therapeutic regulation of endothelial. dysfunction in type 2 diabetes mellitus[J].Invited review,2007,4(2):89-102.

[3]Jiang JL,Zhang XH,Li NS,et al.Probucol decreases asymmetrical dimethylarginine level by alternation of protein arginine methyltransferase I and dimethylarginine dimethylaminohydrolase activity[J].Cardiovasc Drugs Ther,2006,20(4):281-294.

[4]Kirkby NS,Hadoke PW,Bagnall AJ,et al.The endothelin system as a therapeutic target in cardiovascular disease: great expectations or bleak house?[J].Br J Pharmacol,2008,153(6):1105-1119.

[5]成永霞,刘贵波,郭素芬,等.AGEs诱发体外大鼠心脏微血管内皮细胞iNOS表达[J].基础医学与临床,2010,30(5):515-519.

[6]Guzik TJ,Mussa S,Gastaldi D,et al.Mechanisms of increased vascular superoxide production in human diabetes mellitus: role of NAD(P)H oxidase and endothelial nitrieoxide synthase[J].Circulation,2002,105(14):1658-1662.

备注/Memo

备注/Memo:
收稿日期:2011-11-25.基金项目:黑龙江省青年科学基金项目资助(QC2010040);黑龙江省2011年研究生创新科研资金项目资助(YJSCX2011-299HLJ);牡丹江医学院科学技术研究项目资助(2010-16) 通讯作者:杨向红,教授,主要从事糖尿病和心血管疾病机制研究 Email:xhy4933@vip.sina.com 作者简介:成永霞,讲师,博士 Email:cyxgirl2003@163.com
更新日期/Last Update: 2012-05-02