FULLEROL alleviates myocardial ischemia-reperfusion injury by reducing inflammation and oxidative stress in cardiomyocytes via activating the Nrf2/HO-1 signaling pathway

被引：33
作者：
Ding, M. [1 ]
Li, M. [2 ]
Zhang, E-M [3 ]
Yang, H-L [4 ]
机构：
[1] Jilin Univ, Dept Cardiol, China Japan Union Hosp, Jilin Prov Key Lab Genet Diag Cardiovasc Dis,Jili, Changchun, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Clin Lab, Changchun, Peoples R China
[3] Hebei North Univ, Affiliated Hosp 1, Dept Cardiol, Zhangjiakou, Peoples R China
[4] Jilin Univ, China Japan Union Hosp, Dept Emergency, Changchun, Peoples R China
来源：
EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES | 2020年 / 24卷 / 18期
关键词：
Myocardial ischemia-reperfusion injury; Nrf2/HO-1; Inflammatory factors; Cardiomyocyte; ROS;
D O I：
10.26355/eurrev_202009_23056
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
OBJECTIVE: Myocardial ischemia-reperfusion injury (MIRI) is myocardial tissue injury caused by blood supply returning to myocardial tissue after ischemia or hypoxia. The purpose of this study was to investigate the protective effect of FULLEROL on myocardial tissue in MIRI rats and its mechanism. MATERIALS AND METHODS: We use rats and ligate their left anterior descending coronary artery to make a MIRI model, and we also subcutaneously injected some MIRI rats with FULLEROL daily for two weeks before modeling. We determined the effects of model building and the therapeutic effect of FULLEROL on MIRI by detecting the changes of myocardial tissue morphology, myocardial injury markers and cardiac function in rats. In addition, we detected the expression changes of inflammatory factors and antioxidative molecules in rat myocardial tissue and serum to determine the effect of FULLEROL on inflammation and oxidative stress in myocardial tissue. Finally, we detected the activity of the Nrf2/HO-1 signaling pathway in rat cardiomyocytes to determine the mechanism of action of FULLEROL. RESULTS: The structure of myocardial tissue in MIRI rats was remarkably damaged, and the range of myocardial infarction was increased. In addition, the concentrations of creatine kinase and lactate dehydrogenase were increased, and the heart function was reduced, while FULLEROL could reverse these conditions. In addition, FULLEROL was found to reduce the concentration of the inflammatory factors in rat myocardial tissue and serum, and to increase the expression of antioxidative molecules in myocardial tissue. The Nrf2/HO-1 signaling pathway was found to be related to MIRI and FULLEROL could increase the activity of the Nrf2/HO-1 signaling pathway in cardiomyocytes. CONCLUSIONS: FULLEROL can alleviate MIRI by promoting the activity of the Nrf2/HO-1 signaling pathway to reduce the expression of inflammatory factors in rats and increase the antioxidative capacity of cardiomyocytes.
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收藏
页码：9665 / 9674
页数：10
相关论文
共 21 条
[1]   Protective role of peroxiredoxin-4 in heart failure [J].
Ahmed, Naseer ;
Naseem, Masooma ;
Farooq, Javeria .
CLINICAL SCIENCE, 2020, 134 (01) :71-72
[2]   New concepts in reactive oxygen species and cardiovascular reperfusion physiology [J].
Becker, LB .
CARDIOVASCULAR RESEARCH, 2004, 61 (03) :461-470
[3]   Impact of intravenous exenatide infusion for perioperative blood glucose control on myocardial ischemia-reperfusion injuries after coronary artery bypass graft surgery: sub study of the phase II/III ExSTRESS randomized trial [J].
Besch, Guillaume ;
Perrotti, Andrea ;
Salomon du Mont, Lucie ;
Puyraveau, Marc ;
Ben-Said, Xavier ;
Baltres, Maude ;
Barrucand, Benoit ;
Flicoteaux, Guillaume ;
Vettoretti, Lucie ;
Samain, Emmanuel ;
Chocron, Sidney ;
Pili-Floury, Sebastien .
CARDIOVASCULAR DIABETOLOGY, 2018, 17
[4]   ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection [J].
Cadenas, Susana .
FREE RADICAL BIOLOGY AND MEDICINE, 2018, 117 :76-89
[5]   The Role of Nrf2 in the Response to Normal Tissue Radiation Injury [J].
Cameron, Brent D. ;
Sekhar, Konjeti R. ;
Ofori, Maxwell ;
Freeman, Michael L. .
RADIATION RESEARCH, 2018, 190 (02) :99-106
[6]   Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS [J].
Chouchani, Edward T. ;
Pell, Victoria R. ;
Gaude, Edoardo ;
Aksentijevic, Dunja ;
Sundier, Stephanie Y. ;
Robb, Ellen L. ;
Logan, Angela ;
Nadtochiy, Sergiy M. ;
Ord, Emily N. J. ;
Smith, Anthony C. ;
Eyassu, Filmon ;
Shirley, Rachel ;
Hu, Chou-Hui ;
Dare, Anna J. ;
James, Andrew M. ;
Rogatti, Sebastian ;
Hartley, Richard C. ;
Eaton, Simon ;
Costa, Ana S. H. ;
Brookes, Paul S. ;
Davidson, Sean M. ;
Duchen, Michael R. ;
Saeb-Parsy, Kourosh ;
Shattock, Michael J. ;
Robinson, Alan J. ;
Work, Lorraine M. ;
Frezza, Christian ;
Krieg, Thomas ;
Murphy, Michael P. .
NATURE, 2014, 515 (7527) :431-+
[7]   Fullerol ionic fluids [J].
Fernandes, Nikhil ;
Dallas, Panagiotis ;
Rodriguez, Robert ;
Bourlinos, Athanasios B. ;
Georgakilas, Vasilios ;
Giannelis, Emmanuel P. .
NANOSCALE, 2010, 2 (09) :1653-1656
[8]   Nanoparticle fullerol alleviates radiculopathy via NLRP3 inflammasome and neuropeptides [J].
Jin, Li ;
Ding, Mengmeng ;
Oklopcic, Azra ;
Aghdasi, Bayan ;
Xiao, Li ;
Li, Ziyi ;
Jevtovic-Todorovic, Vesna ;
Li, Xudong .
NANOMEDICINE-NANOTECHNOLOGY BIOLOGY AND MEDICINE, 2017, 13 (06) :2049-2059
[9]   Nrf2 regulates ROS production by mitochondria and NADPH oxidase [J].
Kovac, Stjepana ;
Angelova, Plamena R. ;
Holmstroem, Kira M. ;
Zhang, Ying ;
Dinkova-Kostova, Albena T. ;
Abramov, Andrey Y. .
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS, 2015, 1850 (04) :794-801
[10]  
Krokosz Anita, 2007, Postepy Biochem, V53, P91
123