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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

Cited: 8

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Citations:  Bibtex RefMan EndNote GB/T7714

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

10.1631/jzus.B1200263


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",
volume="14",
number="6",
pages="487-495",
year="2013",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1200263"
}

%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

TY - JOUR
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


Abstract: 
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

Reference

[1]Anand, K.V., Anandhi, R., Pakkiyaraj, M., Geraldine, P., 2011. Protective effect of chrysin on carbon tetrachloride (CCl4)-induced tissue injury in male Wistar rats. Toxicol. Ind. Health, 27(10):923-933.

[2]Baines, C.P., Song, C.X., Zheng, Y.T., Wang, G.W., Zhang, J., Wang, O.L., Guo, Y., Bolli, R., Cardwell, E.M., Ping, P., 2003. Protein kinase Cε interacts with and inhibits the permeability transition pore in cardiac mitochondria. Circ. Res., 92(8):873-880.

[3]Borutaite, V., Brown, G.C., 2003. Mitochondria in apoptosis of ischemic heart. FEBS Lett., 541(1-3):1-5.

[4]Burwell, L.S., Brookes, P.S., 2008. Mitochondria as a target for the cardioprotective effects of nitric oxide in ischemia-reperfusion injury. Antioxid. Redox Signal., 10(3):579-599.

[5]Cao, C.M., Xia, Q., Bruce, I.C., Zhang, X., Fu, C., Chen, J.Z., 2003. Interleukin-2 increases activity of sarcoplasmic reticulum Ca2+-ATPase, but decreases its sensitivity to calcium in rat cardiomyocytes. J. Pharmacol. Exp. Ther., 306(2):572-580.

[6]Gao, Q., Pan, H.Y., Qiu, S., Lu, Y., Bruce, I.C., Luo, J.H., Xia, Q., 2006. Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat. Life Sci., 79(3):217-224.

[7]Gao, Q., Yang, B., Ye, Z.G., Wang, J., Bruce, I.C., Xia, Q., 2007. Opening the calcium-activated potassium channel participates in the cardioprotective effect of puerarin. Eur. J. Pharmacol., 574(2-3):179-184.

[8]Gross, G.J., Auchampach, J.A., 2007. Reperfusion injury: does it exist? J. Mol. Cell. Cardiol., 42(1):12-18.

[9]Halestrap, A.P., Clarke, S.J., Javadov, S.A., 2004. Mitochondrial permeability transition pore opening during myocardial reperfusion—a target for cardioprotection. Cardiovasc. Res., 61(3):372-385.

[10]Hamilton, K.L., 2007. Antioxidants and cardioprotection. Med. Sci. Sports Exerc., 39(9):1544-1553.

[11]Hausenloy, D.J., Maddock, H.L., Baxter, G.F., Yellon, D.M., 2002. Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning? Cardiovasc. Res., 55(3):534-543.

[12]Hausenloy, D., Wynne, A., Duchen, M., Yellon, D., 2004. Transient mitochondrial permeability transition pore opening mediates preconditioning-induced protection. Circulation, 109(14):1714-1717.

[13]He, W., Zhang, F.J., Wang, S.P., Chen, G., Chen, C.C., Yan, M., 2008. Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 9(2):100-108.

[14]Hiebert, L., Ping, T., 1997. Protective effect of dextran sulfate and heparin on adult rat cardiomyocytes damaged by free radicals. J. Mol. Cell. Cardiol., 29(1):229-235.

[15]Hu, Q.W., Liu, G.T., 2006. Effects of bicyclol on dimethylnitrosamine-induced liver fibrosis in mice and its mechanism of action. Life Sci., 79(6):606-612.

[16]Huang, H., Shan, J., Pan, X.H., Wang, H.P., Qian, L.B., Xia, Q., 2007. Carvedilol improved diabetic rat cardiac function depending on antioxidant ability. Diabetes Res. Clin. Pract., 75(1):7-13.

[17]Katoh, H., Nishigaki, N., Hayashi, H., 2002. Diazoxide opens the mitochondrial permeability transition pore and alters Ca2+ transients in rat ventricular myocytes. Circulation, 105(22):2666-2671.

[18]Kroemer, G., 1998. The mitochondrion as an integrator/ coordinator of cell death pathways. Cell Death Differ., 5(6):547.

[19]Liu, G.T., Li, Y., Wei, H.L., Lu, H., Zhang, H., Gao, Y.G., Wang, L.Z., 2005. Toxicity of novel anti-hepatitis drug bicyclol: a preclinical study. World J. Gastroenterol., 11(5):665-671.

[20]Lu, H., Li, Y., 2002. Effects of bicyclol on aflatoxin B1 metabolism and hepatotoxicity in rats. Acta Pharmacol. Sin., 23(10):942-945.

[21]Nakagawa, T., Shimizu, S., Watanabe, T., Yamaguchi, O., Ostu, K., Yamagata, H., Inohara, H., Kubo, T., Tsujimoto, Y., 2005. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. Nature, 434(7033):652-658.

[22]Solaini, G., Harris, D.A., 2005. Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion. Biochem. J., 390(Pt2):377-394.

[23]Sun, H., Liu, G.T., 2006. Chemopreventive effect of bicyclol on malignant transformation of WB-F344 rat liver epithelial cells and its effect on related signal transduction in vitro. Cancer Lett., 236(2):239-249.

[24]Sun, L.N., Shen, J., Su, F., Wang, Q., Zhu, Y.J., Lou, X.E., Liang, H.W., Bruce, I.C., Xia, Q., 2009. Bicyclol attenuates oxidative stress and neuronal damage following transient forebrain ischemia in mouse cortex and hippocampus. Neurosci. Lett., 459(2):84-87.

[25]Swift, L.M., Sarvazyan, N., 2000. Localization of dichlorofluorescin in cardiac myocytes: implications for assessment of oxidative stress. Am. J. Physiol. Heart Circ. Physiol., 278(3):H982-H990.

[26]Tao, X., Lu, L.Q., Xu, Q., Li, S.R., Lin, M.T., 2009. Cardioprotective effects of anesthetic preconditioning in rats with ischemia-reperfusion injury: propofol versus isoflurane. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechno.), 10(10):740-747.

[27]Venardos, K.M., Perkins, A., Headrick, J., Kaye, D.M., 2007. Myocardial ischemia-reperfusion injury, antioxidant enzyme systems, and selenium: a review. Curr. Med. Chem., 14(14):1539-1549.

[28]Wang, H., Li, Y., 2006. Protective effect of bicyclol on acute hepatic failure induced by lipopolysaccharide and d-galactosamine in mice. Eur. J. Pharmacol., 534(1-3):194-201.

[29]Wasilewski, M., Wieckowski, M.R., Dymkowska, D., Wojtczak, L., 2004. Effects of N-acylethanolamines on mitochondrial energetics and permeability transition. Biochim. Biophys. Acta, 1657(2-3):151-163.

[30]Watanabe, T., Owada, S., Kobayashi, H.P., Kawakami, H., Nagaoka, S., Murakami, E., Ishiuchi, A., Enomoto, T., Jinnouchi, Y., Sakurai, J., et al., 2007. Protective effects of MnM2Py4P and Mn-salen against small bowel ischemia/reperfusion injury in rats using an in vivo and an ex vivo electron paramagnetic resonance technique with a spin probe. Transplant. Proc., 39(10):3002-3006.

[31]Yellon, D.M., Hausenloy, D.J., 2007. Myocardial reperfusion injury. N. Engl. J. Med., 357(11):1121-1135.

[32]Zhang, S.Z., Wang, N.F., Xu, J., Gao, Q., Lin, G.H., Bruce, I.C., Xia, Q., 2006. Kappa-opioid receptors mediate cardioprotection by remote preconditioning. Anesthesiology, 105(3):550-556.

[33]Zhao, D.M., Sun, T., Li, Y., 2002. The protective effect of bicyclol on ischemia-reperfusion induced kidney injury in rats. Acta Pharm. Sin., 37(6):412-414 (in Chinese).

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