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Shenmai Injection Improves Hypertensive Heart failure by Inhibiting Myocardial Fibrosis via TGF-β1/Smad Pathway Regulation

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Chinese Journal of Integrative Medicine 2023年第2期29卷 119-126页

作者： HU Si-yuan ZHOU Yao ZHONG Sen-jie YANG Meng HUANG Shu-min LI Lin LI Xin-chun HU Zhi-xi School of Sports Art Hunan University of Chinese MedicineChangsha 410208China College of Health Science Wuhan Sports UniversityWuhan 430079China Department of Medicine Hunan Traditional Chinese Medical CollegeZhuzhouHunan Province 412012China Graduate School Hunan University of Chinese MedicineChangsha 410208China Institute of Chinese Medicine Diagnosis Hunan University of Chinese MedicineChangsha 410208China

Objective: To study effects of Shenmai Injection on hypertensive Heart failure and its mechanism for inhibiting myocardial fibrosis. Methods: Salt-sensitive(Dahl/SS) rats were fed with normal diet(0.3% Na Cl) and the high-salt diet(8% Na Cl) to observe the changes in blood pressure and heart function, as the control group and the model group. Salt-insensitive rats(SS-13BN) were fed with the high-salt diet(8% Na Cl) as the negative control group. After modeling, the model rats were randomly divided into Heart failure(HF) group, Shenmai Injection(SMI) group and pirfenidone(PFD) group by a random number table, with 6 rats in each group. They were given sterilized water, SMI and pirfenidone, respectively. Blood pressure, cardiac function, fibrosis and related molecular expression were detected by sphygmomanometer, echocardiogram, enzyme linked immunosorbent assay(ELISA),hematoxylin-eosin staining, Masson staining, immunofluorescence and qPCR analysis. Results: After high-salt feeding, compared with the control and negative control group, in the model group the blood pressure increased significantly, the left ventricular ejection fraction(LVEF) and left ventricular fraction shortening(LVFS) were significantly reduced, and the serum NT-pro BNP concentration increased significantly(all P<0.05);furthermore,the arrangement of myocardial cells was disordered, the edema was severe, and the degree of myocardial fibrosis was also significantly increased(P<0.05);the protein and m RNA expressions of collagen type Ⅰ(Col Ⅰ) were up-regulated(P<0.05), and the mRNA expressions of transforming growth factor β1(TGF-β1), Smad2 and Smad3 were significantly up-regulated(P<0.05). Compared with HF group, after intervention of Shenmai Injection, LVEF and LVFS increased, myocardial morphology was improved, collagen volume fraction decreased significantly(P<0.05), and the mRNA expressions of Col Ⅰ, TGF-β1, Smad2 and Smad3, as well as Col Ⅰprotein expression, were all significantly down-regulated(all P<0.05). Conclusion: Myocardial fibrosis i

关键词： myocardial fibrosis Heart failure Shenmai Injection transforming growth factorβ1/smad hyperlension

Therapeutic Efficacy of Shexiang Baoxin Pill Combined with Exercise in Patients with Heart failure with Preserved Ejection Fraction: A Single-Center, Double-Blind, Randomized Controlled Trial

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Chinese Journal of Integrative Medicine 2023年第2期29卷 99-107页

作者： LIU Si-pei ZHOU Jian-guan JIN Yan GUO Yan ZHOU Shi-wei LIN Mei-lan ZHANG Jun WANG Xiao-nv GUAN Xia-fei WANG Lei Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese MedicineNanjing 210008China Department of Rehabilitation College of Acupuncture and Moxibustion and Massage Health Preservation and RehabilitationNanjing University of Chinese MedicineNanjing 210023China Division of Cardiovascular Rehabilitation Ruian Hospital of Traditional Chinese MedicineRuianZhejiang Province 325299China Xiyuan Hospital China Academy of Chinese Medical SciencesBeijing 100091China

Objective:To evaluate the therapeutic efficacy of Shexiang Baoxin Pill combined with exercise in Heart failure patients with preserved ejection fraction(HFpEF).Methods:Sixty patients with HFpEF were randomly divided into group A(n=20),receiving Shexiang Baoxin Pill combined with home-based exercise training based on conventional drugs for 12 weeks;group B(n=20),receiving conventional drugs combined with home-based exercise training for 12 weeks;and group C(n=20),receiving conventional drug treatment only.Peak oxygen uptake(peakVO2),anaerobic threshold(AT),6-min walking test(6MWT),Pittsburgh Sleep Quality Index(PSQI),and SF-36 questionnaire(SF-36)results before and after treatment were compared among groups.Results:After the 12-week intervention,patients in group C showed significant declines in peakVO2,AT,6MWT,PSQI,and SF-36 compared with pre-treatment(P<0.01),while groups A and B both showed significant improvements in peakVO2,AT,6MWT,PSQI,and SF-36 results compared with pre-treatment(P<0.01).Compared with group C,patients in groups A and B showed significant improvements in peakVO2,AT,6MWT,PSQI,and SF-36(P<0.01).In addition,patients in group A showed more significant improvements in physical function,role-physical,vitality,and mental health scores on the SF-36 questionnaire,and PSQI scores than those in group B(P<0.01).Conclusions:Exercise training improved exercise tolerance,sleep quality and quality of life(QoL)in patients with HFpEF.Notably,Shexiang Baoxin Pill played an active role in sleep quality and QoL of patients with HFpEF.

关键词： Heart failure preserved ejection fraction exercise training Shexiang Baoxin Pill

Mechanism of Qili Qiangxin Capsule for Heart failure Based on miR133a-Endoplasmic Reticulum Stress

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Chinese Journal of Integrative Medicine 2024年第5期30卷 398-407页

作者： JI Xiao-di YANG Ding CUI Xi-yuan LOU Li-xia NIE Bo ZHAO Jiu-li ZHAO Ming-jing WU Ai-ming Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine Key Laboratory of Chinese Internal Medicine of Ministry of Education and BeijingBeijing 100700China Department of Traditional Chinese Medicine Fuwai HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100037China

Objective:To investigate the pharmacological mechanism of Qili Qiangxin Capsule(QLQX)improvement of Heart failure(HF)based on miR133a-endoplasmic reticulum stress(ERS)pathway.Methods:A left coronary artery ligation-induced HF after myocardial infarction model was used in this study.Rats were randomly assigned to the sham group,the model group,the QLQX group[0.32 g/(kg·d)],and the captopril group[2.25 mg/(kg·d)],15 rats per group,followed by 4 weeks of medication.Cardiac function such as left ventricular ejection fraction(EF),fractional shortening(FS),left ventricular systolic pressure(LVSP),left ventricular end diastolic pressure(LVEDP),the maximal rate of increase of left ventricular pressure(+dp/dt max),and the maximal rate of decrease of left ventricular pressure(–dp/dt max)were monitored by echocardiography and hemodynamics.Hematoxylin and eosin(HE)and Masson stainings were used to visualize pathological changes in myocardial tissue.The m RNA expression of mi R133a,glucose-regulated protein78(GRP78),inositol-requiring enzyme 1(IRE1),activating transcription factor 6(ATF6),X-box binding protein1(XBP1),C/EBP homologous protein(CHOP)and Caspase 12 were detected by RT-PCR.The protein expression of GRP78,p-IRE1/IRE1ratio,cleaved-ATF6,XBP1-s(the spliced form of XBP1),CHOP and Caspase 12 were detected by Western blot.Td T-mediated d UTP nick-end labeling(TUNEL)staining was used to detect the rate of apoptosis.Results:QLQX significantly improved cardiac function as evidenced by increased EF,FS,LVSP,+dp/dt max,-dp/dt max,and decreased LVEDP(P<0.05,P<0.01).HE staining showed that QLQX ameliorated cardiac pathologic damage to some extent.Masson staining indicated that QLQX significantly reduced collagen volume fraction in myocardial tissue(P<0.01).Results from RT-PCR and Western blot showed that QLQX significantly increased the expression of mi R133a and inhibited the m RNA expressions of GRP78,IRE1,ATF6 and XBP1,as well as decreased the protein expressions of GRP78,cleaved-ATF6 and XBP1-s and decreased p-IRE1/IRE1 rati

关键词： Heart failure Qili Qiangxin Capsule miR133a endoplasmic reticulum stress apoptosis

Effects of Buyang Huanwu Decoction on Intestinal Barrier, Intestinal Flora, and Trimethylamine Oxide in Rats with Heart failure

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Chinese Journal of Integrative Medicine 2023年第2期29卷 155-161页

作者： WENG Jie-qiong LI Jie-bai YUAN Meng-fei YAO Ting-ting ZHANG Jing-fang ZENG Yuan-yuan ZHAO Jing LI Ying XU Ke SHEN Xiao-xu Department of Cardiology Dongzhimen Hospital of Beijing University of Chinese MedicineBeijing 100700China Department of Nuclear Medicine Dongzhimen Hospital of Beijing University of Chinese MedicineBeijing 100700China Peking University Sixth Hospital Beijing 100700China

Objective: To explore the mechanisms of Buyang Huanwu Decoction(BYHWD) modulating the gut microbiome and trimethylamine oxide(TAMO) to exert cardioprotective effects. Methods: Ligation of the left anterior descending coronary artery was performed in rats to induce Heart failure(HF). Except for the shamoperation group(n=10), 36 operation-induced models were randomized into 3 groups using a random number table(n=12 in each group): the model group, the BYHWD group(15.02 g/kg BYHWD), and the positive group(4.99 g/kg metoprolol succinate). After 4-week treatment(once daily by gavage), echocardiography was applied to evaluate the cardiac function and the Tei index(the ratio of ventricular isovolumic contraction time(IVCT)and isovolumic diastolic time(IVRT) to ejection time(ET)) was calculated;hematoxylin-eosin(HE) staining was observed to characterize the pathology of the myocardium and small intestinal villi. D-lactic acid was detected by an enzyme-linked immunosorbent assay(ELISA). Expressions of occludin, claudin-1, and zonula occludens(ZO-1) were detected by Western blot. 16S ribosomal ribonucleic acid(16S rRNA) sequencing was used to explore the changes in the intestinal flora. TMAO was detected via liquid chromatography-tandem mass spectrometry(LC-MS/MS). Results: In the echocardiography, the Tei index was considerably lower in the positive and BYHWD groups compared with the model group(P<0.05). Besides, BYHWD improved the pathology of myocardium and small intestine of HF rats and lowered the D-lactic acid content in the serum, when compared with the model group(P<0.05). BYHWD also improved the expression of occludin and claudin-1(P<0.05);in the gut microbiota analysis, BYHWD slowed down modifications in the structure distribution of gut microbiota and regulated the diversity of intestinal flora in HF rats. The content of TMAO in the serum was significantly lowered by BYWHT compared with the model group(P<0.05). Conclusion: BYHWD may delay progression of HF by enhancing the intestinal barrier structure, and regul

关键词： Buyang Huanwu Decoction Heart failure intestinal flora trimethylamine oxide

Structural repurposing of SGLT2 inhibitor empagliflozin for strengthening anti-Heart failure activity with lower glycosuria

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Acta Pharmaceutica Sinica B 2023年第4期13卷 1671-1685页

作者： Yixiang Xu Chao Zhang Kai Jiang Xinchun Yang Feng Chen Zhiyang Cheng Jinlong Zhao Jiaxing Cheng Xiaokang Li Xin Chen Luoyifan Zhou Hao Duan Yunyuan Huang Yaozu Xiang Jian Li State Key Laboratory of Bioreactor Engineering Shanghai Frontiers Science Center of Optogenetic Techniques for Cell MetabolismFrontiers Science Center for Materiobiology and Dynamic ChemistryShanghai Key Laboratory of New Drug DesignSchool of PharmacyEast China University of Science and TechnologyShanghai 200237China Shanghai East Hospital School of Life Sciences and TechnologyTongji UniversityShanghai 200092China East China University of Science and Technology-Tengbai Pharmaceutical Innovative Drugs Joint Research Institute Zhuhai Tengbai Pharmaceutical Co.Ltd.Zhuhai 519000China Hubei Key Laboratory of Genetic Regulation and Integrative Biology School of Life SciencesCentral China Normal UniversityWuhan 430079China Yunnan Key Laboratory of Screening and Research on Anti-pathogenic Plant Resources from West Yunnan College of PharmacyDali UniversityDali 671000China Clinical Medicine Scientific and Technical Innovation Center Shanghai Tenth People's HospitalTongji University School of MedicineShanghai 200092China Key Laboratory of Tropical Biological Resources of Ministry of Education College of PharmacyHainan UniversityHaikou 570228China

Sodium-glucose cotransporter 2(SGLT2)inhibitors have been reapproved for Heart failure(HF)therapy in patients with and without diabetes.However,the initial glucose-lowering indication of SGLT2i has impeded their uses in cardiovascular clinical practice.A challenge of SGLT2i then becomes how to separate their anti-HF activity from glucose-lowering side-effect.To address this issue,we conducted structural repurposing of EMPA,a representative SGLT2 inhibitor,to strengthen anti-HF activity and reduce the SGLT2-inhibitory activity according to structural basis of inhibition of SGLT2.Compared to EMPA,the optimal derivative JX01,which was produced by methylation of C2—OH of the glucose ring,exhibited weaker SGLT2-inhibitory activity(IC_(50)>100 nmol/L),and lower glycosuria and glucose-lowering side-effect,better NHE1-inhibitory activity and cardioprotective effect in HF mice.Furthermore,JX01 showed good safety profiles in respect of single-dose/repeat-dose toxicity and hERG activity,and good pharmacokinetic properties in both mouse and rat species.Collectively,the present study provided a paradigm of drug repurposing to discover novel anti-HF drugs,and indirectly demonstrated that SGLT2-independent molecular mechanisms play an important role in cardioprotective effects of SGLT2 inhibitors.

关键词： Heart failure SGLT2 inhibitor Empagliflozin Structural repurposing NHE1(sodium-hydrogen exchanger 1)

Shexiang Tongxin Dropping Pill Allieviates Heart failure via Extracellula Matrix-Receptor Interaction Pathways Based on RNA-Seq Transcriptomics and Experimental Studies

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Chinese Journal of Integrative Medicine 2023年第7期29卷 600-607页

作者： TAN Ya-fang FU Yu-han ZHANG Min-zhou Intensive Care Research Team of Traditional Chinese Medicine Guangdong Province Hospital of Chinese Medicinethe Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou510006China School of Life Sciences and Biopharmaceutics Guangdong Pharmaceutical UniversityGuangzhou510006China

Objective:To investigate the protective mechanisms of Chinese medicine Shexiang Tongxin Dropping Pills(STDP) on Heart failure(HF).Methods:Isoproterenol(ISO)-induced HF rat model and angiotensin Ⅱ(Ang Ⅱ)-induced neonatal rat cardiac fibroblast(CFs) model were used in the present study.HF rats were treated with and without STDP(3 g/kg).RNA-seq was performed to identify differentially expressed genes(DEGs).Cardiac function was evaluated by echocardiography.Hematoxylin and eosin and Masson’s stainings were taken to assess cardiac fibrosis.The levels of collagen Ⅰ(Col Ⅰ) and collagen Ⅲ(Col Ⅲ) were detected by immunohistochemical staining.CCK8 kit and transwell assay were implemented to test the CFs’ proliferative and migratory activity,respectively.The protein expressions of α-smooth muscle actin(α-SMA),matrix metalloproteinase-2(MMP-2),MMP-9,Col I,and Col Ⅲ were detected by Western blotting.Results:The results of RNA-seq analysis showed that STDP exerted its pharmacological effects on HF via multiple signaling pathways,such as the extracellular matrix(ECM)-receptor interaction,cell cycle,and B cell receptor interaction.Results from in vivo experiments demonstrated that STDP treatment reversed declines in cardiac function,inhibiting myocardial fibrosis,and reversing increases in Col Ⅰ and Col Ⅱ expression levels in the hearts of HF rats.Moreover,STDP(6,9 mg/mL) inhibited the proliferation and migration of CFs exposed to Ang Ⅱin vitro(P<0.05).The activation of collagen synthesis and myofibroblast generation were markedly suppressed by STDP,also the synthesis of MMP-2 and MMR-9,as well as ECM components Col Ⅰ,Col Ⅲ,and α-SMA were decreased in Ang Ⅱ-induced neonatal rats’ CFs.Conclusions:STDP had anti-fibrotic effects in HF,which might be caused by the modulation of ECM-receptor interaction pathways.Through the management of cardiac fibrosis,STOP may be a compelling candidate for improving prognosis of HF.

关键词： Shexiang Tongxin Dropping Pill Heart failure RNA-seq extracellular matrix isoproterenol-induced

Astragaloside Ⅳ for Heart failure: Preclinical Evidence and Possible Mechanisms, A Systematic Review and Meta-Analysis

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Chinese Journal of Integrative Medicine 2023年第7期29卷 626-633页

作者： LI Xing-xing LI Dong CUI Xiao-yun ZHOU Kun LIU Jing LU Jin-jin WU Yang LIN Qian LI Yan Department of Cardiology Dongfang HospitalBeijing University of Chinese MedicineBeijing100078China Department of Cardiology Dongzhimen HospitalBeijing University of Chinese MedicineBeijing100700China

Objective:To explore the cardioprotective effects of astragaloside Ⅳ(AS-Ⅳ) in Heart failure(HF).Methods:PubMed,Excerpta Medica Database(EMBASE),Cochrane Library,Web of Science,Wanfang Database,Chinese Bio-medical Literature and Retrieval System(SinoMed),China Science and Technology Journal Database(VIP),and China National Knowledge Infrastructure(CNKI) were searched from inception to November 1,2021for animal experiments to explore AS-Ⅳ in treating HF in rats or mice. The left ventricular ejection fraction(LVEF),left ventricular fractional shortening(LVFS),left ventricular end-diastolic dimension(LVEDD),left ventricular endsystolic dimension(LVESD),left ventricular weight-to-body weight(LVW/BW) and B-type brain natriuretic peptide(BNP) were recorded.The qualities of included studies were assessed by the risk of bias according to the Cochrane handbook.Meta-analysis was performed using Stata 13.0.Results:Twenty-one articles involving 558 animals were considered.Compared with the control group,AS-Ⅳ improved cardiac function,specifically by increasing LVEF(mean difference(MD)=6.97,95% confidence interval(CI)=5.92 to 8.03,P<0.05;fixed effects model) and LVFS(MD=7.01,95% CI=5.84 to 8.81,P<0.05;fixed effects model),and decreasing LVEDD(MD=-4.24,95% CI=-4.74to-3.76,P<0.05;random effects model) and LVESD(MD-4.18,95% CI=-5.26 to-3.10,P<0.05;fixed effects model).In addition,the BNP and LVW/BW levels were decreased in the AS-Ⅳ treatment group(MD=-9.18,95%CI=-14.13 to-4.22,P<0.05;random effects model;MD=-1.91,95% CI=-2.42 to-1.39,P<0.05;random effects model).Conclusions:AS-Ⅳ is a promising therapeutic agent for HF.However,this conclusion needs to be clinically validated in the future.

关键词： astragaloside IV Heart failure pre-clinical evidence systematic review

Molecular and cellular pathophysiology of circulating cardiomyocyte-specific cell free DNA (cfDNA): Biomarkers of Heart failure and potential therapeutic targets

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Genes & Diseases 2023年第3期10卷 948-959页

作者： Abhi Dutta Moumita Das Ankita Ghosh Santanu Rana Raja Peary Mohan College Integrated Biological Research Facility(RIBRF) Raja Peary Mohan CollegeUttarparaHooghlyWest Bengal 712258India

Pathological cardiac damage during Heart failure is associated with cell death and damage associated molecular patterns (DAMPs) release which triggers a viscous cycle of sterile inflammation to mediate maladaptive cardiac tissue remodelling during the progression to Heart failure. DAMPs like cytokines, chemokines, and nuclear or mitochondrial genomic fragments are released in the pathological myocardium. Interestingly, circulating or cytosolic DNA fragments can play a role in the disease by interaction with nucleic acid sensors expressed in cardiomyocyte and non-myocyte neighbouring cells. The circulating cell free DNA (cfDNA) fragments have been clinically reported as markers for various diseases including cardiovascular pathophysiology. Such cfDNA within the DAMP pool can mediate intra- and inter-cellular signalling cascade to upregulate transcriptional expression of inflammatory mediators and trigger oxidative stress within cells. The cellular role of such genomic equivalents varying with chronic or acute stress might be correlated with the cell death forms encountered in myocardium during disease progression. Thus, cfDNA can be phenotypically correlated as a critical player towards upregulation of pathological processes like interstitial fibrosis, cardiomyocyte contractile dysfunction and cell death. Herein, we review the association of cfDNA with Heart failure and analyse their potential usage as novel and effective therapeutic targets towards augmentation of cardiac function.

关键词： Apoptosis Circulating DNA Fibrosis Heart failure Inflammation Nucleic acid receptor

Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic Heart failure

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Science China(Life Sciences) 2023年第12期66卷 2786-2804页

作者： Shuting Yu ZhiYong Sun Xiuzhu Wang Tiantian Ju Changhao Wang Yingqi Liu Zhezhe Qu KuiWu Liu Zhongting Mei Na Li Meixi Lu Fan Wu Min Huang Xiaochen Pang Yingqiong Jia Ying Li Yaozhi Zhang Shunkang Dou Jianhao Jiang Xin Li Baofeng Yang Weijie Du Department of Pharmacology(The State-Province Key Laboratories of Biomedicine Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150081China Northern Translational Medicine Research and Cooperation Center Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150081China Research Unit of Noninfectious Chronic Diseases in Frigid Zone Chinese Academy of Medical Sciences2019RU070Harbin 150081China Traditional Chinese Medicine School Beijing University of Chinese MedicineBeijing 100029China

Ischemic Heart failure(HF)remains a leading cause of morbidity and mortality.Maintaining homeostasis of cardiac function and preventing cardiac remodeling deterioration are critical to halting HF progression.Methyltransferase-like protein 13(Mettl13)has been shown to regulate protein translation efficiency by acting as a protein lysine methyltransferase,but its role in cardiac pathology remains unexplored.This study aims to characterize the roles and mechanisms of Mettl13 in cardiac contractile function and HF.We found that Mettl13 was downregulated in the failing hearts of mice post-myocardial infarction(MI)and in a cellular model of oxidative stress.Cardiomyocyte-specific overexpression of Mettl13 mediated by AAV9-Mettl13 attenuated cardiac contractile dysfunction and fibrosis in response to MI,while silencing of Mettl13 impaired cardiac function in normal mice.Moreover,Mettl13 overexpression abrogated the reduction in cell shortening,Ca^(2+)transient amplitude and SERCA2a protein levels in the cardiomyocytes of adult mice with MI.Conversely,knockdown of Mettl13 impaired the contractility of cardiomyocytes,and decreased Ca^(2+)transient amplitude and SERCA2a protein expression in vivo and in vitro.Mechanistically,Mettl13 impaired the stability of c-Cbl by inducing lysine methylation of c-Cbl,which in turn inhibited ubiquitination-dependent degradation of SERCA2a.Furthermore,the inhibitory effects of knocking down Mettl13 on SERCA2a protein expression and Ca^(2+)transients were partially rescued by silencing c-Cbl in H_(2)O_(2)-treated cardiomyocytes.In conclusion,our study uncovers a novel mechanism that involves the Mettl13/c-Cbl/SERCA2a axis in regulating cardiac contractile function and remodeling,and identifies Mettl13 as a novel therapeutic target for ischemic HF.

关键词： Heart failure Mettl13 SERCA2a c-Cbl ubiquitination