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CLC number: R331.3

On-line Access: 2013-06-04

Received: 2012-09-26

Revision Accepted: 2012-12-20

Crosschecked: 2013-05-06

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Journal of Zhejiang University SCIENCE B 2013 Vol.14 No.6 P.487-495


Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats

Author(s):  Jie Cui, Zhi Li, Ling-bo Qian, Qin Gao, Jue Wang, Meng Xue, Xiao-e Lou, Iain C. Bruce, Qiang Xia, Hui-ping Wang

Affiliation(s):  Department of Physiology, School of Medicine, Zhejiang University, Hangzhou 310058, China; more

Corresponding email(s):   bioqian@163.com, wanghuiping@zju.edu.cn

Key Words:  Ischemia-reperfusion injury, Cardioprotection, Oxidative stress, Mitochondrial permeability transition pore, Bicyclol

Jie Cui, Zhi Li, Ling-bo Qian, Qin Gao, Jue Wang, Meng Xue, Xiao-e Lou, Iain C. Bruce, Qiang Xia, Hui-ping Wang. Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats[J]. Journal of Zhejiang University Science B, 2013, 14(6): 487-495.

@article{title="Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats",
author="Jie Cui, Zhi Li, Ling-bo Qian, Qin Gao, Jue Wang, Meng Xue, Xiao-e Lou, Iain C. Bruce, Qiang Xia, Hui-ping Wang",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats
%A Jie Cui
%A Zhi Li
%A Ling-bo Qian
%A Qin Gao
%A Jue Wang
%A Meng Xue
%A Xiao-e Lou
%A Iain C. Bruce
%A Qiang Xia
%A Hui-ping Wang
%J Journal of Zhejiang University SCIENCE B
%V 14
%N 6
%P 487-495
%@ 1673-1581
%D 2013
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1200263

T1 - Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats
A1 - Jie Cui
A1 - Zhi Li
A1 - Ling-bo Qian
A1 - Qin Gao
A1 - Jue Wang
A1 - Meng Xue
A1 - Xiao-e Lou
A1 - Iain C. Bruce
A1 - Qiang Xia
A1 - Hui-ping Wang
J0 - Journal of Zhejiang University Science B
VL - 14
IS - 6
SP - 487
EP - 495
%@ 1673-1581
Y1 - 2013
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1200263

Objective: To investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion (IR) injuries and its possible mechanism. Methods: Male Sprague-Dawley rats were intragastrically administered with bicyclol (25, 50 or 100 mg/(kg∙d)) for 3 d. Myocardial IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 h. Left ventricular hemodynamics was continuously monitored. At the end of reperfusion, myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and serum lactate dehydrogenase (LDH) level and myocardial superoxide dismutase (SOD) activity were determined by spectrophotometry. Isolated ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR injuries. After reperfusion, cell viability was determined with trypan blue; reactive oxygen species (ROS) and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent probe. The mitochondrial permeability transition pore (mPTP) opening induced by Ca2+ (200 μmol/L) was measured with the absorbance at 520 nm in the isolated myocardial mitochondria. Results: Low dose of bicyclol (25 mg/(kg∙d)) had no significant improving effect on all cardiac parameters, whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR (P<0.05). Medium dose of bicyclol (50 mg/(kg∙d)) markedly improved the myocardial contractility, left ventricular myocyte viability, and SOD activity, as well decreased infarct size, serum LDH level, ROS production, and mitochondrial membrane potential in rat myocardium exposed to IR. The reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/(kg∙d) bicyclol (P<0.05 vs. IR), but not by 25 mg/(kg∙d) bicyclol. The opening of mPTP evoked by Ca2+ was significantly inhibited by medium bicyclol. Conclusions: bicyclol exerts cardioprotection against IR injury, at least, via reducing oxidative stress and its subsequent mPTP opening.

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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