scholarly journals Energy Metabolism Mechanism of Anticardiogenic Shock Effect Component Ginsenoside Rc of Shenfu Injection on H9c2 Myocardial Injury Cells Induced by Hypoxia/Reoxygenation

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yu Chen ◽  
Yan Li ◽  
Guoliang Xu ◽  
Guangbin Shang ◽  
Hongning Liu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cardiogenic Shock ◽  
Myocardial Injury ◽  
Time Effect ◽  
Dose Effect ◽  
Myocardial Cells ◽  
Atp Content ◽  
Shenfu Injection ◽  
H9c2 Cardiomyocytes ◽  
Ginsenoside Rc

Shenfu Injection (SFI) is a common drug used to treat cardiovascular diseases and has a significant effect on cardiogenic shock. Ginsenoside Rc (G-Rc) was an anticardiogenic shock effect component of SFI screened by UHPLC-Q-TOF/MS and multivariate statistical analysis and further selected by molecular docking experiment in our previous study. However, most studies on SFI in the treatment of cardiogenic shock focus on the overall efficacy, and little is known about its effective component on energy metabolism in hypoxia/reoxygenation- (H/R-) induced myocardial injury cells. Therefore, the present study was performed to investigate the dose-effect and time-effect relationship of G-Rc in protecting hypoxic injury of H9c2 cardiomyocytes, and its mechanism on the energy metabolism-related indicators, i.e., adenosine triphosphate (ATP) content, lactate dehydrogenase (LDH) release, and creatine kinase (CK) activity of the myocardial cells, was explored. In this paper, a stable and reliable H/R model of H9c2 cardiomyocytes was established. Compared with the control group, the activity of cardiomyocytes in the H/R group was significantly reduced (P<0.01). The dose-effect and time-effect studies showed that G-Rc could significantly increase cell viability at certain point compared with the H/R group (P<0.01), and the optimum intervention dose and time was 3.33 μmol/L for 12 h. The results concerning energy metabolism mechanism demonstrated that G-Rc pretreatment could improve ATP content, attenuate the LDH leakage, and decrease CK activity and apoptosis rate of H/R cardiomyocytes. Taken together, our findings suggest that G-Rc pretreatment can significantly protect myocardial cells from H/R injury. In addition, G-Rc is able to improve the energy metabolism ability of the injury cardiomyocytes by direct synthesis of ATP and reducing the activity of LDH, CK, and apoptosis rate. These results indicate that G-Rc may be a promising therapeutic candidate for the treatment of cardiovascular disease caused by myocardial H/R injury.

scholarly journals The MicroRNA-210/Casp8ap2 Pathway Alleviates Hypoxia-Induced Injury in Myocardial Cells by Regulating Apoptosis and Autophagy

2020 ◽  
Vol 23 (6) ◽  
pp. E797-E802
Author(s):  
Kunsheng Li ◽  
Jun Pan ◽  
Qiuchang Li ◽  
Shiliang Li ◽  
Kai Li ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Caspase 3 ◽  
Transfection Efficiency ◽  
Beclin 1 ◽  
Caspase 8 ◽  
H9c2 Cells ◽  
Myocardial Cells ◽  
Western Blot Assay ◽  
H9c2 Cardiomyocytes ◽  
Associated Proteins

Aim: This study was conducted to investigate the role of the miR-210/Caspase8ap2 pathway in apoptosis and autophagy in hypoxic myocardial cells. Methods: The miR-control, miR-210 mimic, and miR-210 inhibitor were transfected into rat myocardial H9C2 cells. The transfection efficiency of exogenous miR-210 was determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). H9C2 cells were then treated with CoCl2 for 24, 48, and 72 h to generate a myocardial injury model. The apoptosis of H9C2 cells was assessed by flow cytometry. Additionally, a western blot assay was used to determine the expression of the autophagy-associated proteins light chain 3 (LC3), p62 and Beclin-1, and apoptosis-associated proteins Caspase8ap2, cleaved caspase 8, and cleaved caspase 3. Results: We determined that a 48 h hypoxia treatment duration in H9C2 cardiomyocytes induced myocardial injury. Additionally, the overexpression of miR-210 significantly inhibited cell apoptosis. MiR-210 suppressed autophagy by upregulating p62 and downregulating LC3II/I in hypoxic H9C2 cells. Caspase8ap2 was a putative target of miR-210, miR-210 mediated apoptosis, and autophagy of H9C2 cells via suppressing Caspase8ap2. Furthermore, the expression of caspase 8, caspase 3, and Beclin-1 were decreased in response to miR-210. Conclusion: miR-210 exhibits anti-apoptosis and anti-autophagy effects, which alleviate myocardial injury in response to hypoxia.

scholarly journals MicroRNA-210 Modulates the Cellular Energy Metabolism Shift During H2O2-Induced Oxidative Stress by Repressing ISCU in H9c2 Cardiomyocytes

2017 ◽  
Vol 43 (1) ◽  
pp. 383-394 ◽  
Author(s):  
Wei Sun ◽  
Lei  Zhao ◽  
Xianjing  Song ◽  
Jichang  Zhang ◽  
Yue  Xing ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Complex I ◽  
Cluster Assembly ◽  
Iron Sulfur Cluster ◽  
Myocardial Energy Metabolism ◽  
Cellular Energy ◽  
Atp Assay ◽  
Cellular Energy Metabolism ◽  
H9c2 Cardiomyocytes

Background/Aims: The myocardial energy metabolism shift is one of the most important pathological features of ischemic heart disease (IHD). Although several microRNAs (miRs) are involved in the regulation of myocardial energy metabolism, their exact effects and underlying mechanisms remain unclear. The aim of this study was to investigate whether microRNA(miR-210) regulates the energy metabolism shift during oxidative stress in H9c2 cardiomyocytes. Methods: Cell survival was analyzed via CCK assay. The energy metabolism shift was detected by lactate assay, ATP assay and RT2 profiler glucose metabolism PCR array. Protein and mRNA expression levels were determined by western blot and qPCR. We also used kits to detect the activity of Complex I, Sirt3 and the NAD+/NADH ratio. Results: We determined that miR-210 promoted the energy metabolism shift. The iron-sulfur cluster assembly protein (ISCU) was a target of miR-210. Additionally, we detected the activity of complex I and found that miR-210 inhibits mitochondrial respiration. Interestingly, miR-210 may also indirectly regulate SIRT3 by regulating ISCU. Conclusion: Our results confirm that miR-210 is essential and sufficient for modulating the cellular energy metabolism shift during H2O2-induced oxidative stress in H9c2 cardiomyocytes by targeting ISCU.

scholarly journals Role of Thrombospondin-1 in Sepsis-Induced Myocardial Injury

2021 ◽  
Author(s):  
YUN XIE ◽  
JIAXIANG ZHANG ◽  
WEI JIN ◽  
RUI TIAN ◽  
Ruilan Wang
Keyword(s):  
Mrna Expression ◽  
Real Time ◽  
Quantitative Pcr ◽  
Myocardial Injury ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Expression Level ◽  
Myocardial Cells ◽  
Thrombospondin 1 ◽  
Myocardial Cell Injury

Abstract Objective: Sepsis often causes myocardial injury with a high mortality. We wanted to investigate the effects of thrombospondin-1 (THBS1) expression on myocardial cell injury, oxidative stress and apoptosis in sepsis.Methods: The expression of THBS1 mRNA in LPS-induced mouse primary cardiomyocytes was detected by real-time fluorescence quantitative PCR. We constructed a eukaryotic siRNA expression vector and used liposome transfection to knockdown THBS1 mRNA expression in myocardial cells. We detected the THBS1 mRNA expression level using real-time fluorescent quantitative PCR. Four groups were used: control, LPS, THBS1 siRNA, and LPS + THBS1 siRNA. ELISA was used to detect cTnI, proBNP, ROS, caspase3 and other indicators of cell damage. At the same time, sepsis mouse models were prepared for H&E, TUNEL and caspase-3 staining to evaluate myocardial cell injury and apoptosis. Clinical samples were collected to analyze the serum THBS1 level and correlate it with the prognosis of patients with myocardial injury of sepsis.Results: The expression level of THBS1 mRNA in myocardial cells induced by LPS was increased, and the serum THBS1 level in patients with myocardial injury in sepsis was also significantly increased. In the THBS1 siRNA group with myocardial injury, the levels of cTnI and proBNP were significantly decreased, the levels of the inflammatory cytokines IL-6 and TNF-α were significantly decreased, ROS were significantly decreased, and caspase3 was significantly decreased, and myocardial cell apoptosis was also reduced in the sepsis mouse model. Conclusion: THBS1 is closely related to the biological behavior of myocardial cells and may be a therapeutic target for myocardial injury in sepsis.

scholarly journals Hemodynamic Characteristics of Patients with Myocardial Injury and Cardiogenic Shock Caused by Severe COVID-19-Related Pneumonia

2021 ◽  
Vol Volume 14 ◽  
pp. 9647-9655
Author(s):  
Yongjun Liu ◽  
Yuee Chen ◽  
Jie Chen ◽  
Yukung Kuang ◽  
Niandi Tan ◽  
...  
Keyword(s):  
Cardiogenic Shock ◽  
Myocardial Injury ◽  
Hemodynamic Characteristics

scholarly journals LncRNA KCNQ1OT1 attenuates sepsis-induced myocardial injury via regulating miR-192-5p/XIAP axis

2020 ◽  
Vol 245 (7) ◽  
pp. 620-630 ◽  
Author(s):  
Fangyuan Sun ◽  
Weifang Yuan ◽  
Hao Wu ◽  
Gang Chen ◽  
Yuxia Sun ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Myocardial Dysfunction ◽  
Health Care Systems ◽  
Cardiac Injury ◽  
Convincing Evidence ◽  
Luciferase Reporter ◽  
H9c2 Cardiomyocytes ◽  
Care Systems

Myocardial dysfunction is a prime cause of death in sepsis. This study is to delve into the function of lncRNA KCNQ1OT1 in myocardial injury induced by sepsis. Sepsis-induced myocardial injury model in rat was initiated by intraperitoneally injecting of LPS (10 mg/kg) in vivo, and cardiomyocyte H9c2 was treated with LPS to mimic sepsis in vitro. KCNQ1OT1 and miR-192-5p expressions were detected by qRT-PCR. The cell viability was probed with CCK-8 experiment and the apoptosis of the cardiomyocytes was tested using flow cytometry analysis. Western blot was operated to determine apoptosis-related proteins expressions. ELISA was used to evaluate the levels of TNF-α, IL-6, and IL-1β. Bioinformatics analysis, RT-PCR, dual luciferase reporter assay, and RNA immunoprecipitation experiment were utilized to detect the interrelation of genes. Herein, we proved that KCNQ1OT1 was considerably down-regulated, whereas miR-192-5p was markedly increased in myocardial tissues of septic rats. KCNQ1OT1 interrelated with miR-192-5p, and negatively modulated its expression levels. Overexpression of KCNQ1OT1 or the transfection of miR-192-5p inhibitors greatly facilitated the viability and impeded the apoptosis of H9c2 cardiomyocytes. miR-192-5p paired with the 3ʹUTR of XIAP, and repressed its protein expression, and XIAP was modulated positively by KCNQ1OT1. In conclusion, our work indicates that down-regulation of KCNQ1OT1 advances cardiac injury through regulating miR-192-5p/XIAP axis during sepsis. Impact statement Sepsis-induced cardiomyopathy remains to be a major challenge to health care systems around the globe. There are no known therapies currently available that can cure the disease. This study provides convincing evidence that KCNQ1OT1 could attenuate sepsis-mediated myocardial injury. We further demonstrate that the beneficial function of KCNQ1OT1 was achieved by regulating the miR-192-5p/XIAP axis. We therefore found a new mechanism of cardioprotective effect of KCNQ1OT1, one which also offers a novel theoretical basis for the therapy of sepsis-induced cardiomyopathy.

scholarly journals A importância das intervenções de enfermagem ao paciente com infarto agudo do miocárdio

2013 ◽  
pp. 5
Author(s):  
Dayane Caroline Carvalho ◽  
Débora Cristina Tibúrcio Pareja ◽  
Luiz Faustino dos Santos Maia
Keyword(s):  
Nursing Care ◽  
Myocardial Injury ◽  
Mortality Rates ◽  
Nursing Interventions ◽  
Myocardial Cells ◽  
Acute Myocardial Injury ◽  
Success Of Treatment ◽  
Fast Acting ◽  
Infarto De Miocardio ◽  
Care System

As doenças cardiovasculares possui grande relevância nas taxas de mortalidade e aumento no número de hospitalizações, essas doenças acometidas por diversos fatores devem ser tratadas imediatamente após o aparecimento dos primeiros sintomas. Este estudo teve como objetivo analisar quais intervenções de enfermagem que são adotadas nas unidades de urgência e emergência em pacientes com suspeita de infarto agudo do miocárdio e descrever a importância das intervenções e levantar os principais diagnósticos de enfermagem segundo NANDA. Trata-se de uma pesquisa de revisão bibliográfica descritiva com análise qualitativa, os dados foram coletados nas Bases de Dados de Enfermagem (BDENF) da Biblioteca Virtual de Saúde (BVS) e livros publicados no período de 2009 a 2012. O infarto agudo do miocárdio pode ser definido como um processo pelo qual áreas de células do miocárdio são destruídas de forma permanente. Diagnosticar precocemente o infarto do miocárdio e iniciar os cuidados emergenciais aumenta a chance de sobrevida do paciente infartado. Uma atuação rápida e eficiente do enfermeiro é imprescindível para o sucesso do tratamento e a importância da implementação da sistematização da assistência de enfermagem, possibilitando um cuidado integral ao paciente de forma segura.Descritores: Infarto Agudo do Miocárdio, Intervenções de Enfermagem, Sistematização da Assistência de Enfermagem. The importance of nursing interventions for patients with acute myocardial injutyAbstract: Cardiovascular disease is highly relevant in mortality rates and an increase in the number of hospitalizations diseases affected by several factors must be addressed immediately after the onset of symptoms. This study aimed to analyze which nursing interventions are adopted in the units and emergency patients with suspected to acute myocardial injury and to describe the importance of interventions and to raise the main second NANDA. It is a bibliographic, descriptive and qualitative study the data were collected on the Basis of Data of Nursing (BDENF) of the Virtual Health Library (BVS) and in books which was published in 2009 to 2012. Acute myocardial injury can be defined as a process which areas of myocardial cells are permanently destroyed. Early diagnosis and emergency care increases patients´ survival. A fast acting and effective nursing is essential to the success of treatment and the importance of implementing the nursing care system, providing comprehensive care to patients safely.Descriptors: Acute Myocardial Injury, Nursing Interventions, Nursing Care System. La importância de las intervenciones de enfermería en pacientes con infarto agudo de miocardioResumen: La enfermedad cardiovascular es altamente relevante en las tasas de mortalidad y un aumento en el número de hospitalizaciones, estas enfermedades deben ser tratadas inmediatamente después de la aparición de los síntomas. Este estudio tuvo como objetivo analizar las intervenciones de enfermería se adoptan en las unidades de emergencia y los pacientes con sospecha de infarto agudo de miocardio y describir la importancia de las intervenciones y plantear los principales intervenciones segundo diagnósticos de enfermería de la NANDA. Se trata de un estudio de análisis cualitativo, descriptivo y bibliográfico, se recogieron datos sobre la Base de Datos de Enfermería (BDENF) de la Biblioteca Virtual en Salud (BVS) y los libros publicados entre 2009-2012. Infarto agudo de miocardio se puede definir como un proceso por el cual las áreas de las células miocárdicas se destruyen de forma permanente. El diagnóstico precoz de infarto de miocardio e iniciar la atención de emergencia aumenta las posibilidades de supervivencia de los pacientes con infarto de miocardio. Una enfermera actuación rápida y eficaz es esencial para el éxito del tratamiento y la importancia de la aplicación de la sistematización de la asistencia de enfermería, de atención integral a los pacientes de forma segura.Descriptores: Infarto Agudo del Miocardio, Intervenciones de Enfermería, Sistema de Atención de Enfermería.

Abstract 14455: Hidden in Plain Sight: An Elusive Cause of Cardiogenic Shock

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sarah Chuzi ◽  
Anjan Tibrewala ◽  
Fei Li Kuang ◽  
Benjamin Freed ◽  
Esther Vorovich ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Mitral Valve ◽  
Cardiogenic Shock ◽  
Myocardial Injury ◽  
Hypereosinophilic Syndrome ◽  
Cardiac Biomarkers ◽  
Primary Data ◽  
Circulatory Support ◽  
Chronic Obstructive ◽  
Coronary Syndrome

A 54-year-old man with chronic obstructive pulmonary disease (COPD) presented with three days of chest pain, dyspnea on exertion, and orthopnea. Physical examination revealed jugular venous distention and lower extremity edema. Cardiac biomarkers were elevated. The differential diagnosis for the clinical presentation included: acute coronary syndrome, and type II myocardial infarction or myocardial injury due to acute decompensated heart failure. External records demonstrated recurrent admissions for similar signs and symptoms, with negative coronary angiogram. Shortly after admission, the patient developed acute cardiogenic shock requiring venoarterial extracorporeal membrane oxygenation. Echocardiogram revealed biventricular failure and a possible mitral valve vegetation. The differential diagnosis was refined to include myocarditis (infectious and noninfectious causes), bacterial versus marantic endocarditis, and infiltrative cardiomyopathies. Transesophageal echocardiography revealed mass-like, bileaflet thickening of the mitral valve, not consistent with true vegetation. Infectious, rheumatologic, and hypercoagulable workups were negative. Given the lack of a unifying diagnosis, a right ventricular (RV) endomyocardial biopsy was pursued. This revealed myocardial necrosis and fibrosis, and a mural thrombus with extensive eosinophils. The primary data was then revisited, which revealed history of peripheral eosinophilia that was intermittently suppressed by steroids given for COPD. Cardiac magnetic resonance imaging (MRI) demonstrated diffuse biventricular subendocardial late gadolinium enhancement and RV thrombi. Evaluation for underlying causes of eosinophilia was negative leading to the diagnosis of Loeffler’s endocarditis due to idiopathic hypereosinophilic syndrome. This case demonstrates: (1) the important role of cardiac MRI in the evaluation of both unexplained myocardial injury and new cardiomyopathy, (2) a rare case of Loeffler’s endocarditis requiring mechanical circulatory support, and (3) the consequences of both availability bias and failure to fully “unpack” the primary diagnostic data, which rendered the true etiology of the patient’s cardiogenic shock “hidden in plain sight.”

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