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

Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2013年第6期14卷 487-495页

作者： Jie CUI Zhi LI Ling-bo QIAN Qin GAO Jue WANG Meng XUE Xiao-e LOU Iain C.BRUCE Qiang XIA Hui-ping WANG Department of Physiology School of MedicineZhejiang University Department of Physiology Xuzhou Medical College Department of Physiology Zhejiang Medical College

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(Pcardioprotection against IR injury,at least,via reducing oxidative stress and its

关键词： Ischemia-reperfusion injury cardioprotection Oxidative stress Mitochondrial permeability transition pore Bicyclol

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Protein kinase A-mediated cardioprotection of Tongxinluo relates to the inhibition of myocardial inflammation, apoptosis, and edema in reperfused swine hearts

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Chinese Medical Journal 2013年第8期126卷 1469-1479页

作者： LI Xiang-dong YANG Yue-jin CHENG Yu-tong DOU Ke-fei TIAN Yi MENG Xian-min Department of Evidence Based MedicineState Key Laboratory ofCardiovascular Diseases Fuwai Hospital National Center forCardiovascular Diseases Chinese Academy of Medical Sciencesand Peking Union Medical College Beijing 100037 China Department otCardiologyState Key Laboratory ofCardiovascular Diseases Fuwai Hospital National Center tbrCardiovascular Diseases Chinese Academy of Medical Sciencesand Peking Union Medical College Beijing I00037 China Experimental Animal CenterState Key Laboratory ofCardiovascular Diseases Fuwai Hospital National Center tbrCardiovascular Diseases Chinese Academy of Medical Sciencesand Peking Union Medical College Beijing I00037 China Core LaboratoryState Key Laboratory ofCardiovascular Diseases Fuwai Hospital National Center tbrCardiovascular Diseases Chinese Academy of Medical Sciencesand Peking Union Medical College Beijing I00037 China Department of Cardiology Beijing An Zhen Hospital CapitalMedical University Beijing 100029 China

Background Our previous studies have demonstrated that Tongxinluo （TXL）, a traditional Chinese medicine, can protect hearts against no-reflow and reperfusion injury in a protein kinase A （PKA）-dependent manner. The present study was to investigate whether the PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis. Methods In a 90-minute ischemia and 3-hour reperfusion model, minipigs were randomly assigned to sham, control, TXL （0.05 g/kg, gavaged one hour prior to ischemia）, and TXL ＋ H-89 （a PKA inhibitor, intravenously and continuously infused at 1.0 μg/kg per minute） groups. Myocardial no-reflow, necrosis, edema, and apoptosis were determined by pathological and histological studies. Myocardial activity of PKA and myeloperoxidase was measured by colorimetric method. The expression of PKA, phosphorylated cAMP response element-binding protein （p-CREB）（Ser133）, tumor necrosis factor a （TNF-a）, P-selectin, apoptotic proteins, and aquaporins was detected by Western blotting analysis. Results TXL decreased the no-reflow area by 37.4% and reduced the infarct size by 27.0% （P〈0.05）. TXL pretreatment increased the PKA activity and the expression of Ser133 p-CREB in the reflow and no-reflow myocardium （P 〈0.05）. TXL inhibited the ischemia-reperfusion-induced elevation of myeloperoxidase activities and the expression of TNF-a and P-selectin, reduced myocardial edema in the left ventricle and the reflow and no-reflow areas and the expression of aquaporin-4, -8, and -9, and decreased myocytes apoptosis by regulation of apoptotic protein expression in the reflow and no-reflow myocardium. However, addition of the PKA inhibitor H-89 counteracted these beneficial effects of TXL. Conclusion PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis in the reflow and no-reflow myocardium.

关键词： myocardial inlarction reperfusion therapy, Chinese herbal drugs cardioprotection

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Activation of Akt and cardioprotection against reperfusion injury are maximal with only five minutes of sevoflurane postconditioning in isolated rat hearts

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2013年第6期14卷 511-517页

作者： Yuan-yuan YAO Man-hua ZHU Feng-jiang ZHANG Chuan-yun WEN Lei-lei MA Wen-na WANG Can-can WANG Xian-bao LIU Li-na YU Ling-bo QIAN Jian-an WANG Min YAN Department of Anesthesiology the Second Affiliated HospitalSchool of MedicineZhejiang University Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Department of Cardiology the Second Affiliated HospitalSchool of MedicineZhejiang University Department of Physiology Zhejiang Medical College

It had been proved that administration of sevoflurane for the first two minutes of reperfusion effectively protects the heart against reperfusion injury in rats in vivo.Our aim was to investigate the duration of effective sevoflurane administration and its underlying mechanism in isolated rat hearts exposed to global ischemia/reperfusion(I/R) injury.Adult male Sprague-Dawley rats were randomly divided into six groups(n=12):a sham-operation group,an I/R group,and four sevoflurane postconditioning groups(S2,S5,S10,and S15).In the S2,S5,S10,and S15 groups,the duration times of sevoflurane administration were 2,5,10,and 15 min after the onset of reperfusion,respectively.The isolated rat hearts were mounted on the Langendorff system,and after a period of equilibrium were subjected to 40 min global ischemia and 120 min reperfusion.Left ventricular(LV) hemodynamic parameters were monitored throughout each experiment and the data at 30 min of equilibrium and 30,60,90,and 120 min of reperfusion were analyzed.Myocardial infarct size at the end of reperfusion(n=7 in each group) and the expression of myocardial phosphorylated Akt(p-Akt) after 15-min reperfusion were determined in a duplicate set of six groups of rat hearts(n=5 in each group).Compared with the I/R group,the S5,S10,and S15 groups had significantly improved left ventricular end-diastolic pressure(LVEDP),left ventricular developed pressure(LVDP),and the maximal rate of rise or fall of the LV pressure(±dP/dtmax),and decreased myocardial infarct size(Pcardioprotection against I/R injury in isolated rat hearts.

关键词： Sevoflurane postconditioning Ischemia/reperfusion(I/R) injury cardioprotection Duration of administration Akt

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Pim-1 Kinase Regulating Dynamics Related Protein 1 Mediates Sevoflurane Postconditioning-induced cardioprotection

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Chinese Medical Journal 2017年第3期130卷 309-317页

作者： Jin-Dong Liu Hui-Juan Chen Da-Liang Wang Hui Wang Qian Deng Department of Anesthesiology The Affiliated Hospital of Xuzhou Medical University Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical University Xuzhou Jiangsu 221004 China Department of Anesthesiology Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical University Xuzhou Jiangsu 221004 China

Background： It is well documented that sevoflurane postconditioning （SP） has a significant myocardial protection effect. However, the mechanisms underlying SP are still unclear. In the present study, we investigated the hypothesis that the Pim-1 kinase played a key role in SP-induced cardioprotection by regulating dynamics-related protein 1 （Drpl）. Methods： A Langendorff model was used in this study. Seventy-two rats were randomly assigned into six groups as follows： CON group, ischemia reperfusion （I/R） group, SP group, SP＋proto-oncogene serine/threonine-protein kinase 1 （Pim-1） inhibitor II group, SP＋dimethylsufoxide group, and Pim- 1 inhibitor II group （n = 12, each）. Hemodynamic parameters and infarct size were measured to reflect the extent of myocardial 1/R injury. The expressions ofPim-1, B-cell leukemia/lymphoma 2 （Bcl-2） and cytochrome C （Cyt C） in cytoplasm and mitochondria, the Drp 1 in mitochondria, and the total Drp I and p-Drp I^sor637 were measured by Western blotting. In addition, transmission electron microscope was used to observe mitochondrial morphology. The experiment began in October 2014 and continued until July 2016. Results： SP improved myocardial I/R injury-induced hemodynamic parametric changes, cardiac function, and preserved mitochondrial phenotype and decreased myocardial infarct size （24.49 ± 1.72% in Sev group compared with 41.98 ± 4.37% in I/R group; P 〈 0.05）. However, Pim-1 inhibitor II significantly （P 〈 0.05） abolished the protective effect of SP. Western blotting analysis demonstrated that, compared with I/R group, the expression of Pim-1 and Bcl-2 in cytoplasm and mitochondria as well as the total p-Drplset637 in Sev group （P 〈 0.05） were upregulated. Meanwhile, SP inhibited Drp 1 compartmentalization to the mitochondria followed by a reduction in the release ofCyt C. Pretreatment with Pim- 1 inhibitor II significantly （P 〈 0.05） abolished SP-induced Pim- 1/p-Drp 1^ser637 signaling activation. Conclusions： These findings suggested that SP could attenuate myocardial ischemia-

关键词： cardioprotection Ischemia-reperfusion Injury Mitochondria Pim-1 Postconditioning Sevoflurane

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Wnt/Glycogen Synthase Kinase 3β/β-catenin Signaling Activation Mediated Sevoflurane Preconditioning-induced cardioprotection

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Chinese Medical Journal 2015年第17期128卷 2346-2353页

作者： Jin-Dong Liu Qian Deng Huan-Huan Tian Yun-Ting Pang Gan-Lin Deng Department of Anesthesiology The Affiliated Hospital of Xuzhou Medical College Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Xuzhou Jiangsu 221004 China Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Xuzhou Jiangsu 221004 China

Background： Sevoflurane preconditioning （SP） has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Writ/glycogen synthase kinase 3β（GSK3β）/β-catenin signaling pathway. Methods： Two models were established： A Langendorffperfused rat heart model and the H9C2 cell hypoxia/reoxygenation model. Both rats and H9C2 cells were randomly divided into 6 groups as follows： S group, ischemia-reperfusion （I/R） group, DMSO group, IWP group, SP group, and SP ＋ IWP group. Hemodynamic parameters, lactate dehydrogenase （LDH） activity in coronary effluent and cell culture supernatant, and the infarct size were measured to evaluate myocardial ischemia-reperfusion injuries. To determine the activity of Wnt/GSK3β/β-catenin signaling pathway, the expressions of Wnt3a, phospho-GSK3β, and β-catenin were measured by Western blotting. Results： SP improved cardiac function recovery, reduced infarct size （18 ±2% in the SP group compared with 35 ± 4% in the 1/R group; P 〈 0.05）, decreased LDH activity in coronary effluent, and culture supematant. IWP-2, an inhibitor of Wnt, abolished the cardioprotection by SR In addition, Western blotting analysis demonstrated that the expressions of Wnt3a, phospho-GSK3β, and β-catenin significantly （P 〈 0.05） increased in the I/R group, compared with the S group; and compared to I/R group, SP significantly （P 〈 0.05） increased Wnt3a, phospho-GSK3 β, and β-catenin expressions. Pretreatment with IWP-2 significantly （P 〈 0.05） abolished SP-induced Wnt/GSK3β/β-catenin signaling activation. Conclusions： The results showed for the first time that cardioprotection afforded by SP may be mediated partly via the Wnt/GSK3β/β-catenin signaling pathway.

关键词： cardioprotection Ischemia-reperfusion Injury Preconditioning Sevoflurane Wnt/Glycogen Synthase Kinase3β/β-catenin Signaling

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Late cardioprotection of exercise preconditioning against exhaustive exercise-induced myocardial injury by up-regulatation of connexin 43 expression in rat hearts

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Asian Pacific Journal of Tropical Medicine 2015年第8期8卷 646-651页

作者： Kai Wang Bai-Chao Xu Hai-Yun Duan Hua Zhang Fu-Song Hu College of Sports Science Qufu Normal University Department of Physical Education Hainan Medical University QiongZhou University Physical Test Room

Objective: To investigate the expression of myocardium connexin 43(Cx43) in late exercise preconditioning(LEP) cardioprotection. Methods: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups(n=8). Myocardial injury was judged in accordance with serum levels of c Tn and NT-pro BNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 m RNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting. Results: The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 m RNA level between the four groups. Cx43 protein level was decreased significantly in group EE(P<0.05). However, LEP produced a significant increase in Cx43 protein level(P<0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP(P<0.05). Conclusions: LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43.

关键词： Exercise preconditioning Exhaustive exercise Myocardial injury cardioprotection Connexin 43

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Effects of dexmedetomidine on cardioprotection and other postoperative complications in elderly patients after cardiac and non-cardiac surgerie

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World Journal of Meta-Analysis 2022年第1期10卷 25-36页

作者： Yang-Liang Yang Bao-Ji Hu Jing Yi Meng-Zhi Pan Peng-Cheng Xie Hong-Wei Duan Department of Anesthesia Pudong HospitalShanghai 201399China Department of Anesthesiology Fudan University Pudong Medical CenterFudan UniversityShanghai 201399China

BACKGROUND After cardiac and non-cardiac surgeries,elderly patients have a high probability of developing cardiac complications and postoperative delirium.Although several clinical trials have investigated whether perioperative intravenous dexmedetomidine can protect the heart and reduce postoperative complications such as delirium in elderly patients,the obtained results have been inconsistent.We conducted a meta-analysis to investigate the effects of dexmedetomidine on cardioprotection and other postoperative complications in elderly patients undergoing cardiac or non-cardiac surgery.AIM To investigate the effects of dexmedetomidine on cardiac complications and delirium in elderly patients undergoing cardiac or non-cardiac surgery.METHODS The PubMed,Cochrane Library,web of science,and other sources were comprehensively searched for all randomized controlled trials published before May 2021 that investigated the efficacy of dexmedetomidine in the prevention of cardiac and postoperative delirium(POD).RESULTS In total,18 studies involving 1025 patients were included in the meta-analysis.Intravenous dexmedetomidine significantly reduced cardiac troponin I(cTnI)and the inflammatory factor tumor necrosis factor-α(TNF-α)was comparable to the control group.Dexmedetomidine also reduced the POD and mortality rates.However,patients in the dexmedetomidine group were more likely to have a decreased heart rate(within the normal range)and hypotension during dexmedetomidine administration than those in the control group.There was no difference in the occurrence of myocardial infarction,bradycardia,or stroke between the two groups.Dexmedetomidine significantly shortened the time to extubate;however,it did not shorten the length of stay in the intensive care unit.CONCLUSION The administration of dexmedetomidine during cardiac and non-cardiac surgeries can provide myocardial protection by inhibiting inflammation and cTnI,which may be beneficial for the rapid recovery of patients.Meanwhile,the administration of dexmedetomidine red

关键词： Dexmedetomidine cardioprotection Postoperative delirium Complication Meta-analysis

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Beyond cardiomyocytes:Cellular diversity in the heart's response to exercise

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运动与健康科学(英文) 2023年第4期12卷 423-437,F0003页

作者： Lena E.Trager Margaret Lyons Alexandra Kuznetsov Cedric Sheffield Kangsan Roh Rebecca Freeman James Rhee J.Sawalla Guseh Haobo Li Anthony Rosenzweig Corrigan Minehan Heart Center Division of CardiologyCardiovascular Research CenterDepartment of MedicineMassachusetts General HospitalHarvard Medical SchoolBostonMA 02114USA University of Minnesota Medical School MinneapolisMI 55455USA Department of Anesthesiology and Critical Care Massachusetts General HospitalHarvard Medical SchoolBostonMA 02115USA Institute for Heart and Brain Health University of Michigan Medical CenterAnn ArborMI 48109USA

Cardiomyocytes comprise~70%to 85%of the total volume of the adult mammalian heart but only about 25%to 35%of its total number of cells.Advances in single cell and single nuclei RNA sequencing have greatly facilitated investigation into and increased appreciation of the potential functions of non-cardiomyocytes in the heart.While much of this work has focused on the relationship between non-cardiomyocytes,disease,and the heart's response to pathological stress,it will also be important to understand the roles that these cells play in the healthy heart,cardiac homeostasis,and the response to physiological stress such as exercise.The present review summarizes recent research highlighting dynamic changes in non-cardiomyocytes in response to the physiological stress of exercise.Of particular interest are changes in fibrotic pathways,the cardiac vasculature,and immune or inflammatory cells.In many instances,limited data are available about how specific lineages change in response to exercise or whether the changes observed are functionally important,underscoring the need for further research.

关键词： Angiogenesis Cardiac fibrosis cardioprotection Hypertrophy Non-cardiomyocytes Proliferation

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cardioprotection Afforded by Norepinephrine-mediated Postconditioning in Isolated Rat Hearts

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South China Journal of Cardiology 2008年第3期9卷 143-149页

作者：黄新华李岱张一帅李年生陈本美彭军李元建 Department of Pharmacology School of Pharmaceutical Sciences Central South University Analytical Testing Center of Xiang-Ya Medical College Central South University

Objectives Previous studies have demonstrated that endogenous norepinephrine （NE） plays an important role in the mediation of ischemic preconditioning. The present study is designed to determine whether NE is also involved in mediation of the protective effects of postconditioning. Methods The rat hearts were rapidly excised under anesthesia and attached to a Langendorff apparatus via the aorta for retrograde perfusion with Krebs-Henseleit buffer solution. All hearts were subjected to 30 min of left coronary artery occlusion followed by 60 min of reperfusion, except the control group. Animals were randomly divided into 5 groups as follows：（1） control group, the hearts were underwent same procedures without ischemic insult ; （2） ischemia reperfusion group, the left coronary artery was occluded for 30 rain and followed by 60 min of reperfusion ; （3） ischemic postconditioning （IPost） group, immediately at the onset of reperfusion, the heart was initiated with 1 min of full coronary flow, followed by 1 min of re-occlusion, repeated for a total of three cycles; （4） IPost plus prazosin group, the heart was perfused with prazosin for 10 min before ischemia; （5） IPost plus reserpine group, a single dose of reserpine was administered by i.m. injection, 24 hours before the experiment. Coronary flow was measured by timed collection of coronary effluent and sample of coronary effluent at 5 min of reperfusion were collected for the measurement of creatine kinase （CK）. Infarct size and risk area were determined at the end of experiments. Results 30 min of ischemia and followed by 60 rain of reperfusion caused a significant decrease in cardiac function and a significant increase in CK release and infarct size. Postconditioning with three cycles of 1-min ischemia and 1-min reperfusion markedly improved cardiac function and reduced CK release and infarct size. However, the cardioprotection afforded by postconditioning was abolished by prazosin （10^-6M） , a selective α adrenergic receptor antagonist, or by pretreatment with reser

关键词： postconditioning norepinephrine cardioprotection rat

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Cardioprotective mechanism of SGLT2 inhibitor against myocardial infarction is through reduction of autosis

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Protein & Cell 2022年第5期13卷 336-359页

作者： Kai Jiang Yue Xu Dandan Wang Feng Chen Zizhuo Tu Jie Qian Sheng Xu Yixiang Xu John Hwa Jian Li Hongcai Shang Yaozu Xiang Shanghai East Hospital School of Life Sciences and TechnologyTongji UniversityShanghai 200092China State Key Laboratory of Bioreactor Engineering Shanghai Key Laboratory of New Drug DesignEast China University of Science and TechnologyShanghai 200237China Section of Cardiovascular Medicine Department of Internal MedicineYale Cardiovascular Research CenterYale University School of MedicineNew HavenCT 06511USA Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing Dongzhimen Hospital Affiliated to Beijing University of Chinese MedicineBeijing 100700China

Sodium-glucose cotransporter 2(SGLT2)inhibitors reduce cardiovascular mortality in patients with diabetes mellitus but the protective mechanism remains elusive.Here we demonstrated that the SGLT2 inhibitor,Empagliflozin(EMPA),suppresses cardiomyocytes autosis(autophagic cell death)to confer cardioprotective effects.Using myocardial infarction(Ml)mouse models with and without diabetes mellitus,EMPA treatment significantly reduced infarct size,and myocardial fibrosis,thereby leading to improved cardiac function and survival.In the context of ischemia and nutritional glucose deprivation where autosis is already highly stimulated,EMPA directly inhibits the activity of the Na^(+)/H^(+)exchanger 1(NHE1)in the cardiomyocytes to regulate excessive autophagy.Knockdown of NHE1 significantly rescued glucose deprivation-induced autosis.In contrast,overexpression of NHE1 aggravated the cardiomyocytes death in response to starvation,which was effectively rescued by EMPA treatment.Furthermore,in vitro and in vivo analysis of NHE1 and Beclin 1 knockout mice validated that EMPA s cardioprotective effects are at least in part through downregulation of autophagic flux.These findings provide new insights for drug development,specifically targeting NHE1 and autosis for ventricular remodeling and heart failure after Ml in both diabetic and non-diabetic patients.

关键词： myocardial infarction SGLT2 inhibitors empagliflozin cardioprotection NHE1 autosis

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