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1.
Article in Chinese | WPRIM | ID: wpr-879038

ABSTRACT

Myocardial ischemia-reperfusion injury(MIRI) is an urgent problem in clinical treatment. As cardiomyocytes are terminal cells, MIRI-induced cardiomyocyte death will irreversibly damage the structure and function of the heart. In previous studies, apoptosis was considered to be the only way to regulate cell death, while necrosis could not be regulated. However, current studies have shown that cell necrosis could also be regulated, which was collectively called programmed cell death(PCD). Regulated cell death is actively mediated through molecular pathways, so there is the possibility of inhibiting this signaling to reduce MIRI. At present, PCD mainly includes apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. As a unique treature in China, traditional Chinese medicine has the advantages of multiple pathways, multiple targets, low toxicity, less side effects and low economic costs. With the in-depth study of the efficacy of traditional Chinese medicine against MIRI, it has been confirmed that traditional Chinese medicine could regulate PCD to reduce MIRI. Therefore, this paper focuses on the relationship between PCD and MIRI, and new studies on intervention with relevant traditional Chinese medicine, with the aim to provide new MIRI prevention and treatment methods from the perspective of "intervention of PCD".


Subject(s)
Apoptosis , China , Humans , Medicine, Chinese Traditional , Myocardial Reperfusion Injury/genetics , Myocytes, Cardiac
2.
Article in Chinese | WPRIM | ID: wpr-877651

ABSTRACT

OBJECTIVE@#To observe the effect of electroacupuncture (EA) preconditioning at heart meridian acupoints on the contents of dopamine (DA) and 5-hydroxytryptamine (5-HT) in lateral hypothalamus area (LHA) and cerebellar fastigial nucleus (FN) in the rats with acute myocardial ischemia-reperfusion injury (MIRI), and explore the role and mechanism of LHA and FN in the effect of EA at heart meridian acupoints against acute MIRI.@*METHODS@#Sixty SD rats were randomly divided into a sham-operation group, a model group, an EA heart meridian group and an EA lung meridian group, 12 rats in each group, as well as an LHA plus heart meridian group (damage of bilateral LHA) and an FN plus heart meridian group (damage of bilateral FN), 6 rats in each one. Three days after nucleus destruction, EA was applied to "Shenmen" (HT 7) and "Tongli" (HT 5) in the EA heart meridian group, the LHA plus heart meridian group and the FN plus heart meridian group and EA was applied to "Taiyuan" (LU 9) and "Lieque" (LU 7) in the EA lung meridian group, with 1 V in stimulating voltage and 2 Hz in frequency, lasting 20 minutes each time, once a day, for consecutively 7 days before model replication. Except in the sham-operation group, MIRI rat models were duplicated by ligation of the left anterior descending branch of the coronary artery in the rest groups. Using Power lab physiological recorder, ST segment displacement value was recorded before modeling, 30 min after ligation and 120 min after reperfusion separately. The high performance liquid chromatography-electrochemical detection and analysis system was adopted to determine the contents of DA and 5-HT in LHA and FN dialysate after rat modeling in each group.@*RESULTS@#In comparison of ST segment displacement value 30 min after ligation and 120 min after reperfusion among groups, the value in the model group was higher than that in the sham-operation group (@*CONCLUSION@#EA preconditioning at heart meridian acupoints can effectively alleviate myocardial injury in acute MIRI rats, during which, DA and 5-HT in LHA and FN may be the important material basis.


Subject(s)
Acupuncture Points , Animals , Cerebellar Nuclei , Dopamine , Electroacupuncture , Hypothalamic Area, Lateral , Myocardial Ischemia , Myocardial Reperfusion Injury/therapy , Rats , Rats, Sprague-Dawley , Serotonin
3.
CorSalud ; 12(2): 214-218,
Article in Spanish | LILACS | ID: biblio-1133612

ABSTRACT

RESUMEN La N-acetilcisteína es conocida en varias especialidades médicas. Su empleo en cardiología se ha incrementado desde hace décadas, por su potencial para disminuir el impacto del daño por reperfusión en el infarto miocárdico agudo. Pero el espectro de sus efectos es aún mayor, tiene acciones sobre los radicales de oxígeno, con un papel protector, por la vía de los grupos sulfhidrilos de regiones importantes de la membrana celular, los cuales interfieren y tienen efecto en la función endotelial y en los procesos complejos de adhesión como efectos secundarios; así como otros fenómenos del compartimento extravascular. Estos procesos están estrechamente relacionados con el aparato cardiovascular.


ABSTRACT N-acetylcysteine is known in a number of medical specialties and its ability to decrease the impact of reperfusion injury in acute myocardial infarction has boosted its use in cardiology over the past decades. N-acetylcysteine has a far-reaching range of effects since it functions as a protective agent against oxygen radicals through sulfhydryl groups in important regions of the cell membrane that interfere and affect endothelial functioning and complex adhesion processes as side effects; as well as other phenomena of the extravascular compartment. These processes are closely related to the cardiovascular system.


Subject(s)
Acetylcysteine , Myocardial Reperfusion Injury , Reperfusion Injury , Oxidative Stress
4.
CorSalud ; 12(2): 171-183, graf
Article in Spanish | LILACS | ID: biblio-1133607

ABSTRACT

RESUMEN Desde los primeros informes de pacientes infectados con el SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) en la provincia China de Wuhan, la infección por el nuevo coronavirus ha contagiado a más de 4,7 millones de personas y los fallecidos superan los 315000, hasta el 18 de mayo del 2020. La lesión o daño miocárdico queda definido, como la detección de un valor de las troponinas cardíacas (T o I) por encima del percentil 99 del límite superior de referencia. El mecanismo exacto a partir del cual esta infección por el nuevo coronavirus le infringe un daño a las células del corazón no ha quedado totalmente esclarecido; no obstante, numerosos podrían ser los factores a tener en cuenta: desequilibrio entre el aporte y la demanda, la respuesta inflamatoria sistémica, hipoxia, disfunción microvascular y el daño miocárdico directo ocasionado por el virus.


ABSTRACT Since the first reports of patients infected with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) appeared in the Chinese province of Wuhan, the infection by the new coronavirus has infected more than 4.7 millions of people, and the amount of deaths is greater than 315,000, until May 18, 2020. The myocardial injury or damage is defined as the detection of a value of cardiac troponins (T or I) above the 99th percentile of the upper reference limit. The exact mechanism, from which this infection by the new coronavirus causes damage to the heart cells, has not been completely clarified; however, numerous factors could be taken into account: imbalance between the supply and the demand, systemic inflammatory response, hypoxia, microvascular dysfunction and the direct myocardial injury caused by the virus.


Subject(s)
Myocardial Reperfusion Injury , Coronavirus Infections , Peptidyl-Dipeptidase A
5.
Rev. colomb. cardiol ; 27(3): 142-152, May-June 2020. tab, graf
Article in Spanish | LILACS, COLNAL | ID: biblio-1289204

ABSTRACT

Resumen La infección por SARS-CoV2 es una pandemia. Se creía que el primer caso de esta enfermedad ocurrió el 8 de diciembre de 2019 en la provincia de Hubei en China, aunque posteriormente se indicó que el primer caso confirmado por laboratorio ocurrió el 1.( de diciembre de 2019 ante la presencia de un brote de neumonía en 59 pacientes sospechosos en un mercado local de mariscos en Wuhan. No solo produce patología respiratoria, con frecuencia compremete el sistema cardiovascular ya que produce lesión miocárdica, miocarditis, y, con cierta frecuencia, aumenta la descompensación de enfermedades cardiovasculares preestablecidas. En este artículo se trata de dilucidar el componente cardiovascular hasta ahora existente en la literatura y se sugieren algunos pasos a seguir en pacientes con estas enfermedades, acorde con la evidencia actual.


Abstract Infection due to SARS-CoV2 is a pandemic. It is believed that the first case occurred on 8 December 2019 in Hubei province in China, although it was later indicated that the first laboratory-confirmed case occurred on 1 December 2019 due to the presence of an outbreak of suspected pneumonia in 59 patients in a shellfish market in Wuhan. It not only caused a respiratory disease, it often compromised the cardiovascular system since it produces a myocardial lesion, myocarditis, and, less often, increased the decompensation of pre-established cardiovascular diseases. An attempt is made in this article to elucidate the cardiovascular component presented in the current literature, and to suggest some steps to follow in patients with these diseases in accordance with the current evidence.


Subject(s)
Humans , Male , Female , Coronavirus , Heart Failure , Pneumonia , Respiratory Distress Syndrome, Newborn , Myocardial Reperfusion Injury , Severe Acute Respiratory Syndrome , Myocarditis
6.
Arq. bras. cardiol ; 114(1): 78-86, Jan. 2020. tab, graf
Article in English | LILACS | ID: biblio-1055096

ABSTRACT

Abstract Background: Euterpe oleracea Mart. (açaí) is a fruit with high antioxidant capacity and could be an adjuvant strategy to attenuate ischemia-reperfusion injury. Objective: To evaluate the influence of açaí in global ischemia-reperfusion model in rats. Methods: Wistar rats were assigned to 2 groups: Control (C: receiving standard chow; n = 9) and Açaí (A: receiving standard chow supplemented with 5% açaí; n = 10). After six weeks, the animals were subjected to the global ischemia-reperfusion protocol and an isolated heart study to evaluate left ventricular function. Level of significance adopted: 5%. Results: There was no difference between the groups in initial body weight, final body weight and daily feed intake. Group A presented lower lipid hydroperoxide myocardial concentration and higher catalase activity, superoxide dismutase and glutathione peroxidase than group C. We also observed increased myocardial activity of b-hydroxyacyl coenzyme-A dehydrogenase, pyruvate dehydrogenase, citrate synthase, complex I, complex II and ATP synthase in the A group as well as lower activity of the lactate dehydrogenase and phosphofructokinase enzymes. The systolic function was similar between the groups, and the A group presented poorer diastolic function than the C group. We did not observe any difference between the groups in relation to myocardial infarction area, total and phosphorylated NF-kB, total and acetylated FOXO1, SIRT1 and Nrf-2 protein expression. Conclusion: despite improving energy metabolism and attenuating oxidative stress, açai supplementation did not decrease the infarcted area or improve left ventricular function in the global ischemia-reperfusion model.


Resumo Fundamento: Euterpe oleracea Mart. (açaí) é uma fruta com alta capacidade antioxidante e pode ser uma estratégia adjuvante para atenuar a lesão de isquemia-reperfusão. Objetivo: Avaliar a influência do açaí no modelo global de isquemia-reperfusão em ratos. Metodologia: Ratos Wistar foram divididos em 2 grupos: Controle (C: recebendo ração padrão; n = 9) e Açaí (A: recebendo ração padrão suplementada com 5% de açaí; n = 10). Após seis semanas, os animais foram submetidos ao protocolo global de isquemia-reperfusão e a estudo do coração isolado para avaliar a função ventricular esquerda. Nível de significância adotado: 5%. Resultados: Não houve diferença entre os grupos quanto ao peso corporal inicial e final, e a ingestão diária de ração. O grupo A apresentou menor concentração miocárdica de hidroperóxido lipídico e maior atividade de catalase, superóxido dismutase e glutationa peroxidase do que o grupo C. Também observamos aumento da atividade miocárdica da b-hidroxiacil coenzima-A desidrogenase, piruvato desidrogenase, citrato sintase, complexo I, complexo II e ATP sintase no grupo A, bem como menor atividade das enzimas lactato desidrogenase e fosfofructoquinase. A função sistólica foi semelhante entre os grupos, e o grupo A apresentou função diastólica pior que C. Não foram observadas diferenças entre os grupos em relação à área de infarto do miocárdio, e expressão proteica de NF-kB total e fosforilado, e das proteínas FOXO1, SIRT1 e Nrf-2. Conclusão: apesar de melhorar o metabolismo energético e atenuar o estresse oxidativo, a suplementação de açaí não diminuiu a área infartada nem melhorou a função ventricular esquerda no modelo global de isquemia-reperfusão.


Subject(s)
Animals , Male , Rats , Plant Extracts/pharmacology , Myocardial Reperfusion Injury/physiopathology , Oxidative Stress/drug effects , Energy Metabolism/drug effects , Euterpe/chemistry , Oxidative Stress/physiology , Disease Models, Animal , Energy Metabolism/physiology
8.
Article in Chinese | WPRIM | ID: wpr-828880

ABSTRACT

OBJECTIVE@#To investigate the mechanism by which dripping pills (STDP) improves coronary microcirculation disorder (CMD) and cardiac dysfunction in a porcine model of myocardial ischemia-reperfusion injury.@*METHODS@#Fourteen minipigs were randomly selected for interventional balloon occlusion of the middle left anterior descending branch to induce CMD, and another 7 pigs received sham operation. The pig models of CMD were randomized equally into the model group and STDP-treated group. All the animals were fed with common feed for 8 weeks, and in STDP-treated group, the pigs were given STDP at the daily dose of 3 mg/kg (mixed with feed) for 8 weeks. Before and at the 8th week after the operation, the pigs underwent coronary angiography and echocardiography to determine the vessel lumen diameter and TIMI frame count (CTFC). The pathologies of the myocardium and the microvessels were examined with HE staining at the 8th week. Western blotting was used to detect the expression of silencing information regulator (Sirt1), peroxidase proliferator-activated receptor-γ coactivator-1α (PGC-1α), peroxisome proliferator-activated receptor α (PPARα), extracellular signal-regulated kinase1/2 (ERKI/2), Toll-like receptor 4 (TLR4), and uncoupling protein 2 (UCP2) in myocardial tissue.@*RESULTS@#Before and at the 8th week after the operation, the diameter of the anterior descending vessel in the 3 groups did not differ significantly ( > 0.05). At the 8th week, the number of CTFC frames in the model group increased significantly compared with that in the sham-operated group, but was obviously lowered by treatment with STDP ( < 0.05). Myocardial ischemia-reperfusion injury significantly increased the interventricular septal thickness at end-diastole, left ventricular end-diastole dimension, end-diastole volume, interventricular septal thickness at end-systole and left ventricular mass at 8 weeks after the modeling ( < 0.05), but such changes were significantly alleviated by treatment with STDP (P < 0.05). STDP treatment markedly alleviated myocardial microvascular congestion, thrombosis and peripheral inflammatory cell infiltration induced by myocardial ischemia-reperfusion, but atrophy of the myocardial muscle fiber remained distinct. STDP obviously suppressed the down-regulation of Sirt1, PGC-1α, and PPARα and the up-regulation of ERK1/ 2, TLR4, and UCP2 in the myocardial tissues induced by myocardial ischemia-reperfusion injury.@*CONCLUSIONS@#STDP has anti-inflammatory effects and regulates energy metabolism in the myocardium through modulating Sirt1, PGC-1α, PPARα, ERKI/2, TLR4, and UCP2 to improve CMD and cardiac dysfunction after myocardial ischemia-reperfusion.


Subject(s)
Animals , Drugs, Chinese Herbal , Microcirculation , Myocardial Reperfusion Injury , Myocardium , Rats , Rats, Sprague-Dawley , Swine
9.
Article in Chinese | WPRIM | ID: wpr-828517

ABSTRACT

OBJECTIVE@#To investigate the protective effect of melatonin against myocardial ischemia reperfusion (IR) injury in isolated rat hearts and explore the underlying mechanisms.@*METHODS@#The isolated hearts from 40 male SD rats were randomly divided into 4 groups (=10): the control group, where the hearts were perfused with KH solution for 175 min; IR group, where the hearts were subjected to global ischemia for 45 min followed by reperfusion for 120 min; IR+melatonin (Mel+IR) group, where melatonin (5 μmol/L) was administered to the hearts 1 min before ischemia and during the first 5 min of reperfusion, followed by 115 min of reperfusion; and IR+2, 3-butanedione monoxime (IR+BDM) group, where the hearts were treated with BDM (20 mmol/L) in the same manner as melatonin treatment. Myocardial injury in the isolated hearts was assessed based on myocardial injury area, caspase-3 activity, and expressions of cytochrome C and cleaved caspase-3 proteins. Cardiac contracture was assessed using HE staining and by detecting lactate dehydrogenase (LDH) activity and the content of cardiac troponin I (cTnI) in the coronary outflow, measurement of left ventricular end-diastolic pressure (LVEDP) and electron microscopy. The content of ATP in the cardiac tissue was also determined.@*RESULTS@#Compared with those in the control group, the isolated hearts in IR group showed significantly larger myocardial injury area and higher caspase-3 activity and the protein expressions of cytochrome C and cleaved caspase-3 with significantly increased LDH activity and cTnI content in the coronary outflow and elevated LVEDP at the end of reperfusion; HE staining showed obvious fractures of the myocardial fibers and the content of ATP was significantly decreased in the cardiac tissue; electron microscopy revealed the development of contraction bands. In the isolated hearts with IR, treatment with Mel or BDM significantly reduced the myocardial injury area, caspase-3 activity, and protein expressions of cytochrome C and cleaved caspase-3, obviously inhibited LDH activity, lowered the content of cTnI and LVEDP, reduced myocardial fiber fracture, and increased ATP content in the cardiac tissue. Both Mel and BDM inhibited the formation of contraction bands in the isolated hearts with IR injury.@*CONCLUSIONS@#Mel can alleviate myocardial IR injury in isolated rat hearts by inhibiting cardiac contracture, the mechanism of which may involve the upregulation of ATP in the cardiac myocytes to lessen the tear of membrane and reduce cell content leakage.


Subject(s)
Animals , Heart , Male , Melatonin , Pharmacology , Therapeutic Uses , Muscle Contraction , Myocardial Reperfusion Injury , Drug Therapy , Myocytes, Cardiac , Rats , Rats, Sprague-Dawley
10.
Acta Physiologica Sinica ; (6): 433-440, 2020.
Article in Chinese | WPRIM | ID: wpr-827044

ABSTRACT

The aim of the present study was to investigate the effect of zinc transporter Zip2 (SLC39A2) on mitochondrial respiration during myocardial ischemia/reperfusion (I/R) and the underlying mechanisms. An in vivo myocardial I/R model was established in mice by ligation of left anterior descending coronary artery. Cardiac zinc concentration was measured by inductively coupled plasma-optical emission spectrometer (ICP-OES), and the mitochondrial respiratory function and oxidative phosphorylation were determined by high-resolution respirometry (Oxygraph-2K). The phosphorylation levels of STAT3 and ERK in myocardial tissue were detected by Western blot. The results showed that, compared with the sham group, cardiac zinc concentration in myocardium was decreased in wild-type mice and further reduced in Zip2 knockout mice after I/R. Mitochondrial respiratory control rate (RCR) and oxidative phosphorylation were decreased in Zip2 knockout mice and worsened by I/R. Phosphorylation levels of STAT3 (Ser) and ERK were significantly decreased in Zip2 knockout mice after I/R. In I/R myocardial tissue, STAT3 overexpression significantly improved the mitochondrial respiratory function, while STAT3 dominant negative mutant (STAT3 S727A) inhibited mitochondrial respiratory function. Moreover, the impairment of mitochondrial function by Zip2 knockout was reversed by STAT3 overexpression. These results suggest that Zip2 regulates mitochondrial respiration via phosphorylation of STAT3 during myocardial I/R, which may represent the underlying mechanism of Zip2 cardioprotection against I/R injury.


Subject(s)
Animals , Carrier Proteins , Mice , Mice, Knockout , Mitochondria , Myocardial Reperfusion Injury , Myocardium , Myocytes, Cardiac
11.
Braz. j. med. biol. res ; 53(9): 0-0, 2020. tab, graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132553

ABSTRACT

Myocardial ischemia/reperfusion (MI/R) injury is a complex phenomenon that causes severe damage to the myocardium. However, the potential molecular mechanisms of MI/R injury have not been fully clarified. We identified potential molecular mechanisms and therapeutic targets in MI/R injury through analysis of Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were found between MI/R injury and normal samples, and overlapping DEGs were found between GSE61592 and GSE67308. Gene Ontology (GO) and pathway analysis were performed for overlapping DEGs by Database for Annotation, Visualization and Integration Discovery (DAVID). Then, a network of protein-protein interaction (PPI) was constructed through the Search Tool for the Retrieval of Interacting Genes (STRING) database. Potential microRNAs (miRNAs) and therapeutic small molecules were screened out using microRNA.org database and the Comparative Toxicogenomics database (CTD), respectively. Finally, we identified 21 overlapping DEGs related to MI/R injury. These DEGs were significantly enriched in IL-17 signaling pathway, cytosolic DNA-sensing pathway, chemokine signaling, and cytokine-cytokine receptor interaction pathway. According to the degree in the PPI network, CCL2, LCN2, HP, CCL7, HMOX1, CCL4, and S100A8 were found to be hub genes. Furthermore, we identified potential miRNAs (miR-24-3p, miR-26b-5p, miR-2861, miR-217, miR-4251, and miR-124-3p) and therapeutic small molecules like ozone, troglitazone, rosiglitazone, and n-3 polyunsaturated fatty acids for MI/R injury. These results identified hub genes and potential small molecule drugs, which could contribute to the understanding of molecular mechanisms and treatment for MI/R injury.


Subject(s)
Myocardial Reperfusion Injury , MicroRNAs , Computational Biology , Gene Expression Profiling , Gene Regulatory Networks , Protein Interaction Maps , Gene Ontology
12.
Article in Chinese | WPRIM | ID: wpr-828936

ABSTRACT

OBJECTIVE@#To investigate the protective effect of melatonin against myocardial ischemia reperfusion (IR) injury in isolated rat hearts and explore the underlying mechanisms.@*METHODS@#The isolated hearts from 40 male SD rats were randomly divided into 4 groups (=10): the control group, where the hearts were perfused with KH solution for 175 min; IR group, where the hearts were subjected to global ischemia for 45 min followed by reperfusion for 120 min; IR+melatonin (Mel+IR) group, where melatonin (5 μmol/L) was administered to the hearts 1 min before ischemia and during the first 5 min of reperfusion, followed by 115 min of reperfusion; and IR+2, 3-butanedione monoxime (IR+BDM) group, where the hearts were treated with BDM (20 mmol/L) in the same manner as melatonin treatment. Myocardial injury in the isolated hearts was assessed based on myocardial injury area, caspase-3 activity, and expressions of cytochrome C and cleaved caspase-3 proteins. Cardiac contracture was assessed using HE staining and by detecting lactate dehydrogenase (LDH) activity and the content of cardiac troponin I (cTnI) in the coronary outflow, measurement of left ventricular end-diastolic pressure (LVEDP) and electron microscopy. The content of ATP in the cardiac tissue was also determined.@*RESULTS@#Compared with those in the control group, the isolated hearts in IR group showed significantly larger myocardial injury area and higher caspase-3 activity and the protein expressions of cytochrome C and cleaved caspase-3 with significantly increased LDH activity and cTnI content in the coronary outflow and elevated LVEDP at the end of reperfusion; HE staining showed obvious fractures of the myocardial fibers and the content of ATP was significantly decreased in the cardiac tissue; electron microscopy revealed the development of contraction bands. In the isolated hearts with IR, treatment with Mel or BDM significantly reduced the myocardial injury area, caspase-3 activity, and protein expressions of cytochrome C and cleaved caspase-3, obviously inhibited LDH activity, lowered the content of cTnI and LVEDP, reduced myocardial fiber fracture, and increased ATP content in the cardiac tissue. Both Mel and BDM inhibited the formation of contraction bands in the isolated hearts with IR injury.@*CONCLUSIONS@#Mel can alleviate myocardial IR injury in isolated rat hearts by inhibiting cardiac contracture, the mechanism of which may involve the upregulation of ATP in the cardiac myocytes to lessen the tear of membrane and reduce cell content leakage.


Subject(s)
Animals , Contracture , Male , Melatonin , Myocardial Ischemia , Myocardial Reperfusion Injury , Myocardium , Myocytes, Cardiac , Rats , Rats, Sprague-Dawley
13.
Article in Chinese | WPRIM | ID: wpr-880763

ABSTRACT

OBJECTIVE@#To investigate the effect of miR-133b on cardiomyocyte apoptosis induced by myocardial ischemia-reperfusion (I/R) and explore the mechanism.@*METHODS@#Thirty-six adult SD rats were randomized into sham-operated group, I/R group, AdmiR-NC group and AdmiR-133b group, and rat models of myocardial I/R were established in the latter 3 groups with myocardial injections of saline or recombinant adenoviruses in the left ventricle. The expression of MiR-133b was detected using RT-qPCR, and cardiac function of the rats was determined using FDP 1 HRV and BRS analysis system. Serum CK-MB and cTnI levels were determined by ELISA, myocardial injury was evaluated with HE staining, cardiomocyte apoptosis was detected by flow cytometry, and ROS content was determined using a DCFH-DA probe. In the in vitro experiment, H9C2 myocardial cells with hypoxia/reoxygenation (H/R) treatment were transfected with Mir-NC or MiR-133b mimic, and the cellular expression of MiR-133b, cell apoptosis, and ROS content were determined. Dual luciferase reporter assay was performed to verify the targeting relationship between miR-133b and YES1. The effects of pc-YES1 or miR-133b mimic transfection on YES1 expression, apoptosis, and ROS content in H9C2 cells were evaluated.@*RESULTS@#Compared with those in I/R group, miR-133b expression was obviously up-regulated, LVEDP, cTnI and CK-MB levels were significantly decreased, and LVSP, +dp/dt, -dp/dt, HR and CF levels were increased in admiR-133b group (@*CONCLUSIONS@#miR-133b can inhibit I/R-induced myocardial cell apoptosis and ROS accumulation by targeting YES1 to reduce myocardial I/R injury in rats.


Subject(s)
Animals , Apoptosis , MicroRNAs/genetics , Myocardial Reperfusion Injury , Myocytes, Cardiac , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species
14.
Article in English | WPRIM | ID: wpr-880589

ABSTRACT

Cardiomyocytes injury model has been widely used in the study for the molecular mechanism of cardiovascular diseases and drug action. It is very important to select the appropriate model due to the different formation mechanisms for various models. Clinical cardiovascular pathological change is relatively complex. Currently used models according to the characteristics of clinical cardiovascular diseases mainly include hydrogen peroxide-induced myocardial cell damage model, hypoxia reoxygenation injury model, adriamycin-induced myocardial cell damage model, high sugar high fat-induced myocardial cell damage model, and isoprenaline-induced myocardial cell damage model. Every model has its advantages as well as its disadvantages. The suitable model of myocardial cell injury can be selected according to the research purpose.


Subject(s)
Animals , Cell Hypoxia , Myocardial Reperfusion Injury/metabolism , Myocardium , Myocytes, Cardiac/metabolism , Rats , Rats, Sprague-Dawley , Research
15.
Article in English | WPRIM | ID: wpr-880580

ABSTRACT

OBJECTIVES@#Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) controls mitochondrial biogenesis, but its role in cardiovascular diseases is unclear. The purpose of this study is to explore the effect of PGC1α on myocardial ischemia-reperfusion injury and the underlying mechanisms.@*METHODS@#The transverse coronary artery of SD rat was ligated for 30 minutes followed by 2 hours of reperfusion. Triphenyltetrazolium chloride (TTC) staining was performed to measure the area of myocardial infarction. Immunohistochemistry and Western blotting were used to detect the PGC1α expression in myocardium. The rat cardiomyocyte H9C2 was subjected to hypoxia/reoxygenation (H/R) with the knockdown of PGC1α or hypoxia- inducible factor 1α (HIF-1α), or with treatment of metformin. Western blotting was used to detect the expression of PGC1α, HIF-1α, p21, BAX, and caspase-3. CCK-8 was performed to detect cell viability, and flow cytometry was used to detect apoptosis and mitochondrial superoxide (mitoSOX) release. RT-qPCR was used to detect the mRNA expression of PGC1α and HIF-1α. Besides, chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter gene assay were applied to detect the transcriptional regulation effect of HIF-1α on PGC1α.@*RESULTS@#After I/R, the PGC1α expression was increased in infarcted myocardium. H/R induced H9C2 cell apoptosis (@*CONCLUSIONS@#After I/R, HIF-1α up-regulates the expression of PGC1α, leading to an increase in ROS production and aggravation of injury. Metformin can inhibit the accumulation of HIF-1α during hypoxia and effectively protect myocardium from ischemia/reperfusion injury.


Subject(s)
Animals , Apoptosis , Hypoxia-Inducible Factor 1, alpha Subunit/genetics , Myocardial Reperfusion Injury/genetics , Myocytes, Cardiac/metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Rats , Rats, Sprague-Dawley , Reperfusion Injury
16.
Braz. j. med. biol. res ; 53(2): e9106, 2020. graf
Article in English | LILACS | ID: biblio-1055491

ABSTRACT

Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.


Subject(s)
Animals , Rabbits , Myocardial Reperfusion Injury/metabolism , Myocardial Ischemia/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Myocytes, Cardiac/pathology , MicroRNAs/metabolism , PTEN Phosphohydrolase/metabolism , Signal Transduction , Blotting, Western , Disease Models, Animal , Proto-Oncogene Proteins c-akt/metabolism , Real-Time Polymerase Chain Reaction , Flow Cytometry , Mice, Inbred C57BL
17.
Arq. bras. cardiol ; 113(6): 1092-1101, Dec. 2019. tab, graf
Article in English | LILACS | ID: biblio-1055064

ABSTRACT

Abstract Background: Functional assessment to rule out myocardial ischemia using coronary computed tomography angiography (CCTA) is extremely important and data on the Brazilian population are still limited. Objective: To assess the diagnostic performance of myocardial perfusion by CCTA in the detection of severe obstructive coronary artery disease (CAD) compared with single-photon emission computerized tomography (SPECT). To analyze the importance of anatomical knowledge to understand the presence of myocardial perfusion defects on SPECT imaging that is not identified on computed tomography (CT) scan. Method: A total of 35 patients were evaluated by a simultaneous pharmacologic stress protocol. Fisher's exact test was used to compare proportions. The patients were grouped according to the presence or absence of significant CAD. The area under the ROC curve was used to identify the diagnostic performance of CCTA and SPECT in perfusion assessment. P < 0.05 values were considered statistically significant. Results: For detection of obstructive CAD, CT myocardial perfusion analysis yielded an area under the ROC curve of 0.84 [a 95% confidence interval (CI95%): 0.67-0.94, p < 0.001]. SPECT myocardial perfusion imaging, on the other hand, showed an AUC of 0.58 (95% CI 0.40 - 0.74, p < 0.001). In this study, false-positive results with SPECT are described. Conclusion: Myocardial perfusion analysis by CTA displays satisfactory results compared to SPECT in the detection of obstructive CAD. CCTA can rule out false-positive results of SPECT.


Resumo Fundamento: A avaliação funcional para descartar a isquemia miocárdica utilizando a angiotomografia computadorizada (angio-TC) de coronárias é de extrema importância e dados na população brasileira ainda são escassos. Objetivo: Avaliar o desempenho diagnóstico da perfusão miocárdica pela angio-TC de coronárias na detecção de doença arterial coronariana (DAC) obstrutiva significativa em comparação com a tomografia computadorizada por emissão de fóton único (SPECT; do inglês, single photon emission computerized tomography). Analisar a importância do conhecimento anatômico para entender a presença de defeito de perfusão miocárdica pela SPECT que não é identificado pela tomografia computadorizada (TC). Método: Trinta e cinco pacientes foram avaliados por um protocolo de estresse farmacológico simultâneo. O teste exato de Fisher foi utilizado para comparação entre as proporções. Os pacientes foram agrupados de acordo com a presença ou não de DAC significativa. A área sob a curva foi utilizada para identificar o desempenho diagnóstico da avaliação da perfusão pela angio-TC de coronárias e pela SPECT. Os valores de p < 0,05 foram considerados estatisticamente significativos. Resultados: Para detecção de DAC obstrutiva a avaliação da perfusão miocárdica pela TC teve uma área sob a curva de 0,84 [intervalo de confiança de 95% (IC95%): 0,67 a 0,94, p < 0,001]. Já o estudo da perfusão miocárdica pela SPECT foi de 0,58 (IC95%: 0,40 a 0,74, p < 0,001). Neste estudo, foram descritos falso-positivos pela SPECT. Conclusão: A avaliação da perfusão miocárdica pela angio-TC apresenta resultados satisfatórios em comparação com os da SPECT na detecção de DAC obstrutiva. A angio-TC de coronárias tem capacidade de afastar falso-positivos da SPECT.


Subject(s)
Humans , Male , Female , Middle Aged , Coronary Artery Disease/diagnostic imaging , Tomography, Emission-Computed, Single-Photon/methods , Coronary Angiography/methods , Myocardial Perfusion Imaging/methods , Coronary Artery Disease/physiopathology , Cineangiography/methods , Myocardial Reperfusion Injury/physiopathology , Myocardial Reperfusion Injury/diagnostic imaging , ROC Curve , Sensitivity and Specificity , Computed Tomography Angiography
18.
Rev. bras. cir. cardiovasc ; 34(6): 674-679, Nov.-Dec. 2019. tab, graf
Article in English | LILACS | ID: biblio-1057497

ABSTRACT

Abstract Objective: To study the response of myocardial ischemia/reperfusion injury (MI/RI) in rats to simulated geomagnetic activity. Methods: In a simulated strong geomagnetic outbreak, the MI/RI rat models were radiated, and their area of myocardial infarction, hemodynamic parameters, creatine kinase (CK), lactate dehydrogenase (LDH), melatonin, and troponin I values were measured after a 24-hour intervention. Results: Our analysis indicates that the concentrations of troponin I in the geomagnetic shielding+operation group were lower than in the radiation+operation group (P<0.05), the concentrations of melatonin in the shielding+operation group and normal+operation group were higher than in the radiation + operation group (P<0.01), and the concentrations of CK in the shielding + operation group were lower than in the radiation + operation group and normal + operation group (P<0.05). Left ventricular developed pressure (LVDP) and ± dP/dtmax in the radiation+operation group were lower than in the shielding + operation group and normal+operation group (P<0.01). Left ventricular end-diastolic pressure (LEVDP) in the shielding + operation group was higher than in the normal + operation group (P<0.05). There was no significant difference in area of myocardial infarction and LDH between the shielding + operation group and the radiation + operation group. Conclusion: Our data suggest that geomagnetic activity is important in regulating myocardial reperfusion injury. The geomagnetic shielding has a protective effect on myocardial injury, and the geomagnetic radiation is a risk factor for aggravating the cardiovascular and cerebrovascular diseases.


Subject(s)
Animals , Male , Rats , Myocardial Reperfusion Injury/physiopathology , Magnetic Fields/adverse effects , Rats, Sprague-Dawley , Creatine Kinase , Disease Models, Animal , Hemodynamics
19.
Acta cir. bras ; 34(11): e201901104, Nov. 2019. graf
Article in English | LILACS | ID: biblio-1054677

ABSTRACT

Abstract Purpose: Myocardial ischemia/reperfusion (Ml/R) injury is a leading cause of damage in cardiac tissues, with high rates of mortality and disability. Biochanin A (BCA) is a main constituent of Trifolium pratense L. This study was intended to explore the effect of BCA on Ml/R injury and explore the potential mechanism. Methods: In vivo MI/R injury was established by transient coronary ligation in Sprague-Dawley rats. Triphenyltetrazolium chloride staining (TTC) was used to measure myocardial infarct size. ELISA assay was employed to evaluate the levels of myocardial enzyme and inflammatory cytokines. Western blot assay was conducted to detect related protein levels in myocardial tissues. Results: BCA significantly ameliorated myocardial infarction area, reduced the release of myocardial enzyme levels including aspartate transaminase (AST), creatine kinase (CK-MB) and lactic dehydrogenase (LDH). It also decreased the production of inflammatory cytokines (IL-1β, IL-18, IL-6 and TNF-α) in serum of Ml/R rats. Further mechanism studies demonstrated that BCA inhibited inflammatory reaction through blocking TLR4/NF-kB/NLRP3 signaling pathway. Conclusion: The present study is the first evidence demonstrating that BCA attenuated Ml/R injury through suppressing TLR4/NF-kB/NLRP3 signaling pathway-mediated anti-inflammation pathway.


Subject(s)
Animals , Male , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/prevention & control , NF-kappa B/drug effects , Genistein/pharmacology , Toll-Like Receptor 4/drug effects , NLR Family, Pyrin Domain-Containing 3 Protein/drug effects , Aspartate Aminotransferases/blood , Reference Values , Myocardial Reperfusion Injury/metabolism , Signal Transduction/drug effects , Blotting, Western , Reproducibility of Results , Cytokines/blood , NF-kappa B/metabolism , Rats, Sprague-Dawley , Creatine Kinase/blood , Lactate Dehydrogenases/blood , Toll-Like Receptor 4/metabolism , Anti-Inflammatory Agents/pharmacology
20.
Acta cir. bras ; 34(11): e201901106, Nov. 2019. tab, graf
Article in English | LILACS | ID: biblio-1054683

ABSTRACT

Abstract Purpose: To investigate whether GDF11 ameliorates myocardial ischemia reperfusion (MIR) injury in diabetic rats and explore the underlying mechanisms. Methods: Diabetic and non-diabetic rats subjected to MIR (30 min of coronary artery occlusion followed by 120 min of reperfusion) with/without GDF11 pretreatment. Cardiac function, myocardial infarct size, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), superoxide dismutase (SOD) 15-F2tisoprostane, autophagosome, LC3II/I ratio and Belcin-1 level were determined to reflect myocardial injury, oxidative stress and autophagy, respectively. In in vitro study, H9c2 cells cultured in high glucose (HG, 30mM) suffered hypoxia reoxygenation (HR) with/without GDF11, hydrogen peroxide (H2O2) and autophagy inhibitor 3-methyladenine (3-MA) treatment, cell injury; oxidative stress and autophagy were assessed. Results: Pretreatment with GDF11 significantly improved cardiac morphology and function in diabetes, concomitant with decreased arrhythmia severity, infarct size, CK-MB, LDH and 15-F2tisoprostane release, increased SOD activity and autophagy level. In addition, GDF11 notably reduced HR injury in H9c2 cells with HG exposure, accompanied by oxidative stress reduction and autophagy up-regulation. However, those effects were completely reversed by H2O2 and 3-MA. Conclusion: GDF11 can provide protection against MIR injury in diabetic rats, and is implicated in antioxidant stress and autophagy up-regulation.


Subject(s)
Animals , Male , Autophagy/drug effects , Myocardial Reperfusion Injury/metabolism , Myocardial Reperfusion Injury/drug therapy , Oxidative Stress/drug effects , Diabetes Mellitus, Type 1/metabolism , Growth Differentiation Factors/pharmacology , Reference Values , Superoxide Dismutase/analysis , Cardiotonic Agents/pharmacology , Myocardial Reperfusion Injury/pathology , Up-Regulation/drug effects , Cell Line , Blotting, Western , Reproducibility of Results , Rats, Sprague-Dawley , Streptozocin , Microscopy, Electron, Transmission , Diabetes Mellitus, Experimental/metabolism , Hemodynamics/drug effects , Antioxidants/pharmacology
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