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Andrographolide protects against atrial fibrillation by alleviating oxidative stress injury and promoting impaired mitochondrial bioenergetics

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第7期24卷 632-649页

作者： Pengcheng YU Jiaru CAO Huaxin SUN Yingchao GONG Hangying YING Xinyu ZHOU Yuxing WANG Chenyang QI Hang YANG Qingbo LV Ling ZHANG Xia SHENG Department of Cardiology Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang ProvinceSir Run Run Shaw HospitalZhejiang University School of MedicineHangzhou 310016China xinjiang key laboratory of cardiac electrophysiology and remodeling the First Affiliated Hospital of Xinjiang Medical UniversityUrumqi 830011China Department of Cardiology the First School of Clinical Medicine of Zhejiang Chinese Medicine UniversityHangzhou 310006China

Atrial fibrillation(AF)is the most prevalent cardiac arrhythmia seen in clinical settings,which has been associated with substantial rates of mortality and ***,clinically available drugs have limited efficacy and adverse *** aimed to investigate the mechanisms of action of andrographolide(Andr)with respect to *** used network pharmacology approaches to investigate the possible therapeutic effect of *** define the role of Andr in AF,HL-1 cells were pro-treated with Andr for 1 h before rapid electronic stimulation(RES)and rabbits were pro-treated for 1 d before rapid atrial pacing(RAP).Apoptosis,myofibril degradation,oxidative stress,and inflammation were *** sequencing(RNA-seq)was performed to investigate the relevant *** treatment attenuated RAP-induced atrial electrophysiological changes,inflammation,oxidative damage,and apoptosis both in vivo and in ***-seq indicated that oxidative phosphorylation played an important *** electron microscopy and adenosine triphosphate(ATP)content assay respectively validated the morphological and functional changes in *** translocation of nuclear factor erythroid 2-related factor 2(Nrf2)to the nucleus and the molecular docking suggested that Andr might exert a therapeutic effect by influencing the Keap1-Nrf2 *** conclusions,this study revealed that Andr is a potential preventive therapeutic drug toward AF via activating the translocation of Nrf2 to the nucleus and the upregulation of heme oxygenase-1(HO-1)to promote mitochondrial bioenergetics.

关键词： Traditional Chinese medicine Atrial fibrillation Andrographolide Oxidative stress Network pharmacology

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Recombinant adeno-associated virus serotype 9 with p65 ribozyme protects H9c2 cells from oxidative stress through inhibiting NF-κB signaling pathway

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Journal of Geriatric Cardiology 2014年第4期11卷 311-315页

作者： Zhan SUN Yi-Tong MA Bang-Dang CHEN Fen LIU xinjiang key laboratory of Cardiovascular Disease Research Urumqi 830054 Xinjiang Uygur Autonomous Region China laboratory of Functional Experiment Preclinical Medicine Xinjiang Medical University Urumqi 830054 Xinjiang Uygur Autonomous Region China Department of Cardiology the First Affiliated Hospital of Xinjiang Medical University Urumqi 830054 Xinjiang Uygur Autonomous Region China

Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB （NF-κB）. The NF-κB transcription factor family includes several subunits （p50, p52, p65, c-Rel, and Rel B） that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Mechods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme （AAV9-R65-CMV-eGFP） was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the under-lying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65-CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease.

关键词： Cardiomyocytes Adenovirus R65 ribozyme Apoptosis NF-κB pathway

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Ventricular tachycardia as the initial symptom of cardiac hydatidosis

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Chinese Medical Journal 2019年第22期132卷 2765-2766页

作者： Yan-Mei Lu Ling Zhang Qiang Xing Xian-Hui Zhou Yao-Dong Li Jiang-Hua Zhang Tuerhong Zukela Bao-Peng Tang Department of Pacing electrophysiology The First Affiliated Hospital of Xinjiang Medical UniversityUrumqiXinjiang 830054China

To the Editor:A 44-year-old female presented at the local hospital for repeated episodes of having palp Nations,accompanied with cold sweats,amaurosis,vomiting,and limb weakness in the previous 2 *** electrocardiogram indicated "ventricular tachycardia" when she was not feeling *** symptoms alleviated significantly after injections of"amiodarone"(dose unknown),after which the patient was discharged.A local physician recommended ablation,so the patient was transferred to our *** patient was generally healthy and had lived in a region with *** to the patient5 self-report,she had been diagnosed as having liver hydatidosis 30 years ago,but had recovered after surgical treatment at the local ***,the patient claimed to have no other medical history.

关键词： tachycardia transferred claimed

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Changes in microRNAs expression are involved in age-related atrial structural remodeling and atrial fibrillation

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Chinese Medical Journal 2013年第8期126卷 1458-1463页

作者： XU Guo-jun GAN Tian-yi TANG Bao-peng CHEN Zu-heng Mahemuti Ailiman ZHOU Xian-hui JIANG Tao SONG Jian-guo GUO Xia LI Yao-dong MIAO Hai-jun ZHANG Yu LI Jin-xin Department of CardiologyFirst Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China Department ofAnimal Experiment First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China laboratory of electrophysiology First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China Department of Molecular Biology First Affiliated Hospital Xinjiang Medical UniversityUrumqi Xinjiang 830011 China

Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins. However, their role in age-related cardiac remodeling and atrial fibrillation （AF） was not well understood. The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF. Methods Three groups of dogs were studied： adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing. The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction. Pathohistological and ultrastructural changes were tested by light and electron microscopy. Apoptosis index of myocytes was detected by TUNEL. Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes, the accelerated fibrosis, and apoptosis with aging and/or in AF dogs. Compared to the adult group, the expressions of microRNAs-21 and -29 were significantly increased, whereas the expressions of microRNAs-1 and -133 showed obvious downregulation tendency in the aged group. Compared to the aged group, the expressions of microRNAs-1, -21, and -29 was significantly increased in the old group in AF; contrastingly, the expressions of microRNA-133 showed obvious downregulation tendency. Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AE

关键词： atrial fibrillation aging structural remodeling microRNAs

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Patients taking angiotensin-converting enzyme inhibitors/angiotensin II type I receptor blockers:higher risks of severe acute respiratory syndrome coronavirus 2 infection but milder clinical manifestations?

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Chinese Medical Journal 2020年第22期133卷 2650-2652页

作者： Jie-Lin Deng Yun-Qiu Jiang Yan-Kai Guo Hong-Liang Li Department of Cardiology Renmin Hospital of Wuhan UniversityCardiovascular Research InstituteWuhan UniversityHubei Key Laboratory of CardiologyWuhanHubei 430060China Department of Medicine University of Oklahoma Health Sciences CenterOklahoma CityOK 73117USA cardiac Pacing and electrophysiology Department The First Affiliated Hospital of Xinjiang Medical UniversityUrumqiXinjiang 830000China

Recently,there has been an unprecedented interest in the topic of angiotensin converting enzyme 2(ACE2)-associated drugs administration,such as angiotensin-converting enzyme inhibitors(ACEIs)/angiotensin II type I receptor blockers(ARBs),in COVID-19 patients.A recent article put forward the concern that patients taking ACEIs/ARBs were under higher risk of COVID-19 infection.[1]They revealed that expression of ACE2,the receptor for severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)to enter host cells,is up-regulated,thus facilitating the initial viral attachment step of SARS-CoV-2 in these patients.[2]

关键词： ACE2 respiratory acute

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Prediction of atrial fibrillation development and progression:current perspectives

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World Journal of Cardiology 2016年第3期8卷 267-276页

作者： Konstantinos Vlachos Konstantinos P Letsas Panagiotis Korantzopoulos Tong Liu Stamatis Georgopoulos Athanasios Bakalakos Nikolaos Karamichalakis Sotirios Xydonas Michael Efremidis Antonios Sideris Second Department of Cardiology Laboratory of Cardiac Electrophysiology"Evangelismos" General Hospital of Athens First Department of Cardiology University Hospital of Ioannina Tianjin key laboratory of Ionic-Molecular Function of Cardiovascular Disease Department of CardiologyTianjin Institute of CardiologySecond Hospital of Tianjin Medical University

Atrial fibrillation(AF) is the most common arrhythmia in clinical practice. Several conventional and novel predictors of AF development and progression(from paroxysmal to persistent and permanent types) have been reported. The most important predictor of AF progression is possibly the arrhythmia itself. The electrical, mechanical and structural remodeling determines the perpetuation of AF and the progression from paroxysmal to persistent and permanent forms. Common clinical scores such as the hypertension, age ≥ 75 years, transient ischemic attack or stroke, chronic obstructive pulmonary disease, and heart failure and the congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke/transient ischemic attack, vascular disease, age 65-74 years, sex category scores as well as biomarkers related to inflammation may also add important information on this topic. There is now increasing evidence that even in patients with so-called lone or idiopathic AF, the arrhythmia is the manifestation of a structural atrial disease which has recently been defined and described as fibrotic atrial cardiomyopathy. Fibrosis results from a broad range of factors related to AF inducing pathologies such as cell stretch, neurohumoral activation, and oxidative stress. The extent of fibrosis as detected either by late gadolinium enhancement-magnetic resonance imaging or electroanatomic voltage mapping may guide the therapeutic approach based on the arrhythmia substrate. The knowledge of these risk factors may not only delay arrhythmia progression, but also reduce the arrhythmia burden in patients with first detected AF. The present review highlights on the conventional and novel risk factors of development and progression of AF.

关键词： Atrial fibrillation Development Progression Risk factors inflammation Fibrosis

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MiR-101 is involved in atrial electrical remodeling in human persistent atrial fibrillation

MiR-101 is involved in atrial electrical remodeling in human...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：兰欢 Chen Tangting Zeng Bo Zeng Xiaorong key laboratory of Medical electrophysiology Ministry of Educationand the Institute of Cardiovascular ResearchLuzhou Medical College

Background Atrial fibrillation（AF）is the most commonly encountered clinical arrhythmia associated with pronounced morbidity,mortality,and socio-economic *** pathological entity is associated with an altered expression profile of genes that are important for atrial *** RNAs have been investigated to involve in electrical remodeling in atrial fibrillation（AF）.Micro RNA-101（mi R-101）has a high expression level in heart,but the role of mi R-101 in AF remains *** To evaluate the changes of mi R-101 in patients with persistent AF and to find its target *** The right atrial appendage tissue were obtained during cardiac surgery from patients（16 sinus rhythm and 9 persistent AF）.The expression level of mi R-101 was assayed by real time *** effects of mi R-101 on targetgene expression were evaluated in mice which injected mi R-101 *** The expression level of mi R-101 was significantly decreased in persistent AF patients compared with SR *** of mi R-101 mimic in C57 mice resulted in the upregulation of SK3 protein *** Atrial mi R-101 is significantly decreased in AF,leading to SK3 downregulation and possibly contributing to the electrical remodeling in AF.

关键词： MiR-101 atrial fibrillation electrical remodeling

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Total flavonoids from Anchusa italica improves cardiac function and attenuates cardiac remodeling post-myocardial infarction in mice

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中国药理学与毒理学杂志 2019年第9期33卷 698-699页

作者： WANG Shou-bao SONG Jun-ke WANG Rong-rong GAO Li ZHANG Li FANG Lian-hua LYU Yang DU Guan-hua Beijing key laboratory of Drug Targets Identification and Drug Screening Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijingChina Beijing key laboratory of Polymorphic Drugs Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijingChina State key laboratory of Bioactive Substance and Function of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijingChina China key laboratory of Traditional Uygur Medical Prescription Xinjiang Uygur Autonomous Region Institute of Traditional Uygur MedicineUrumqi 830001China

OBJECTIVE The plant of Anchusa italicahas been traditionally used in Uighur medicine for the treatment of cardiovascular and cerebrovascular diseases in *** previous study showed that total flavonoids from Anchusa italica(TFAI)exhibited potent cardioprotection on acute ischemia/reperfusion injured *** study was undertaken to investigate the effects of TFAI on chronic myocardial infarction in mice and the underlying *** Total flavonoids were extracted from the whole herb of Anchusa italica and were characterized using HPLC-MS *** left anterior descending branch of coronary artery was ligated to induce myocardial infarction in *** surgery,the mice were orally fed with TFAI at the doses of 10,30 and 50 mg·kg-1 body mass per day for a total of four *** function and infarct size were measured,and the levels of inflammatory mediators were *** and eosin(HE)stain and Masson Trichrome stain were *** apoptotic factors such as Bax,Bcl-2 and cleaved caspase 3 as well as the key proteins in the PI3K/Akt/mTOR signaling pathway were examined by Western *** The content of total flavonoids in TFAI was 56.2%.Four weeks following the MI surgery,TFAI enhanced the survival rate in post-MI *** administration at the doses of 30 and 50 mg·kg-1 significantly reduced the infarct size and improved cardiac function indicated by elevated EF and *** of inflammation factors showed that the sera levels of TNF-α,IL-1β and IL-6 were significantly decreased by TFAI treatment as compared to the MI *** stain and Masson Trichrome stain demonstrated that TFAI suppressed myocyte hypertrophy and cardiac fibrosis indicated by decreased cross-section area and collagen *** blot analysis showed that cleaved caspase 3 and Bax/Bcl-2 were signifi⁃cantly downregulated following TFAI ***,TFAI treatment significantly suppressed the activation of the PI3K/Akt/mTOR signaling pathway

关键词： total flavonoids Anchusa italica cardiac function

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Contribution of DNA methylation in chronic stress-induced cardiac remodeling and arrhythmias in mice

Contribution of DNA methylation in chronic stress-induced ca...

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2019年中国生理学会心血管生理学术研讨会

作者： Peng Zhang Tao Li Ya-Qin Liu Hao Zhang Si-Meng Xue Hai-Ying Mary Cheng Ji-Min Cao key laboratory of Medical electrophysiology of Ministry of Education and Medical Electrophysiological key laboratory of Sichuan Province Institute of Cardiovascular ResearchCollaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease of Sichuan ProvinceSouthwest Medical University Department of Biology University of Toronto Mississauga key laboratory of Cellular Physiology of Ministry of Education and the Department of PhysiologyShanxi Medical University

Aim:It is recognized that stress can induce cardiac dysfunction,but the underlying mechanisms are not well *** present study aimed to test the hypothesis that chronic negative stress leads to alterations in DNA methylation of certain cardiac genes,which in turn contribute to pathological remodeling of the ***:The mice that were exposed to chronic restraint stress（CRS） for four weeks as animal *** phenotypes were compared non-stress（NS） and CRS mice by ELISA,forced swim test（FST） and sucrose preference test（SPT）,echocardiography,*** representation bisulfite sequencing（RRBS） was to study the DNA methylation in the murine ***-eosin（H-E）,immunofluorescent（IF） staining,western blotting,reverse transcription-quantitative PCR（RT-qPCR） methylation-specific PCR（MSP） were used to verify the ***:We found that mice that were exposed to CRS for four weeks exhibited cardiac remodeling towards heart failure,as characterized by ventricular chamber dilatation,wall thinning and decreased *** also induced cardiac arrhythmias including intermittent sinus tachycardia and bradycardia,frequent premature ventricular contraction,and sporadic atrioventricular conduction *** levels of stress hormones were elevated,and the cardiac expression of tyrosine hydroxylase,a marker of sympathetic innervation,was increased in CRS ***,we found that RRBS although CRS did not lead to global changes in DNA methylation in the murine heart,it nevertheless altered methylation at specific genes that are associated with dilated cardiomyopathy（DCM）（e.g.,Desmin） and adrenergic signaling pathways of cardiomyocytes（ASPC）（e.g.,Adral）.Conclusion:We conclude that CRS induces cardiac remodeling and arrhythmias,potentially through altered methylation of myocardial genes associated with the DCM and ASPC pathways.

关键词： chronic stress cardiac remodeling arrhythmia DNA methylation

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心脏纤维化机制研究的全新视角

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Science Bulletin 2023年第22期68卷 2704-2708页

作者：王海帆杜晓军张幼怡肖晗 Department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalBeijing 100191China State key laboratory of Vascular Homeostasis and remodeling Peking UniversityBeijing 100191China NHC key laboratory of Cardiovascular Molecular Biology and Regulatory Peptides Beijing 100191China Beijing key laboratory of Cardiovascular Receptors Research Beijing 100191China Search Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases Chinese Academy of Medical SciencesBeijing 100191China Institute of Cardiovascular Sciences School of Basic Medical SciencesPeking University Health Science CenterBeijing 100191China Baker Heart and Diabetes Institute Melbourne 8008Australia School of Basic Medical Sciences Xi’an Jiaotong University Health Science Centerand Cardiometabolic Innovation Center(Ministry of Education)Xi’an 710061China key laboratory of xinjiang Endemic and Ethnic Diseases(Ministry of Education) Shihezi University School of MedicineShihezi 832003China

cardiac fibrosis is the excessive deposition of extracellular matrix(ECM)proteins in heart tissues leading to functional and electrophysiological *** a common pathology in different diseased conditions,cardiac fibrosi... 详细信息

关键词：心脏纤维化 pathology cardiac

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