scholarly journals Mechanical Tissue Resuscitation (MTR) reduces myocardial tissue injury following myocardial ischemia‐reperfusion (MI/R)

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
James E. Jordan ◽  
Jennifer J. Mays ◽  
Julie E. Shelton ◽  
Edreca A. Thompson ◽  
Allyson K. Bryant ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Tissue ◽  
Myocardial Ischemia Reperfusion ◽  
Mechanical Tissue

scholarly journals Over-expression of SDF-1α on BMSCs Reduce the Injury Caused by PMN in Myocardial Ischemia/reperfusion

2021 ◽  
Author(s):  
Ruihua Wang ◽  
Wen Wei ◽  
Shuling Rong ◽  
Ting Wang ◽  
Bao Li
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Myocardial Ischemia ◽  
Cell Therapy ◽  
Stem Cell Therapy ◽  
Ischemia Reperfusion ◽  
Myocardial Tissue ◽  
Inflammatory Factor ◽  
Expression Levels ◽  
Myocardial Ischemia Reperfusion

Abstract Background: To study the protective effect of BMSC overexpressing SDF-1α on myocardial ischemia/reperfusion (I/R), to improve the limitation that only part of BMSC is recruited to the site of myocardial injury in the treatment of ischemic heart disease. It provides a new scheme for stem cell therapy for clinical treatment of reperfusion injury.Methods: Collect blood samples from PCI patients and healthy individuals to detect PMN and SDF-1α expression; Construction of BMSC overexpressing SDF-1α (oe-SDF-1α); In the case of no intervention or intervention by BMSC respectively, cell level: the migration ability of PMN to hypoxia/reoxygenation (H/R) cardiomyocytes and the expression of SDF-1α, CXCR4, apoptosis, oxidative stress and other indicators of cardiomyocytes were detected; In vivo level: PMN, SDF-1α, CXCR4, oxidative stress and inflammatory factor levels were detected in I/R mice. And carry out statistical analysis.Results: ① In the clinic, compared with the control group, the expression levels of SDF-1α and PMN in the blood of PCI patients increased. ② Under H/R conditions, cardiomyocytes express and secrete SDF-1α, activate PMN migration and infiltration mediated by SDF-1/CXCR4 signal pathway, promote cardiomyocyte apoptosis and increase the level of oxidative stress; oe-SDF-1α has a stronger ability to migrate to H/R cardiomyocytes and has more repair ability than BMSC.It is more suitable as a tool cell for stem cell therapy. ③ The expression levels of SDF-1α and PMN are increased in I/R mice. oe-SDF-1α can reduce the ability of PMN to reside to the damaged part of myocardial tissue significantly, thereby reducing myocardial tissue damage, oxidative stress, inflammatory factor levels in I/R mice. Conclusions: The SDF-1/CXCR4 biological axis not only plays an important role in BMSC migration, but also helps to enhance the therapeutic effect of BMSC-based therapy. Oe-SDF-1α has a more repairing effect on reducing cell damage caused by PMN, and can be used as a new type of cell for the treatment of IRI.

scholarly journals miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yulin Guo ◽  
Jie Gao ◽  
Yan Liu ◽  
Xitao Zhang ◽  
Xiangguang An ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Signal Pathway ◽  
Expression Level ◽  
Myocardial Tissue ◽  
Ampk Signaling ◽  
Infarct Area ◽  
Myocardial Ischemia Reperfusion

Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury.

Mechanical Tissue Resuscitation Protects Against Myocardial Ischemia-Reperfusion Injury

2013 ◽  
Vol 29 (1) ◽  
pp. 116-123 ◽  
Author(s):  
James E. Jordan ◽  
Jennifer J. Mays ◽  
Julie E. Shelton ◽  
Allyson K. Bryant ◽  
Magan R. Lane ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Mechanical Tissue

Effects of miR-26a-5p and PTEN on Myocardium of Myocardial Ischemia-reperfusion Mice

2021 ◽  
Vol 7 (5) ◽  
pp. 4057-4065
Author(s):  
Lifei Yu ◽  
Shiwen Lu
Keyword(s):  
Myocardial Ischemia ◽  
Caspase 3 ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Myocardial Tissue ◽  
Model Group ◽  
Caspase 9 ◽  
Blank Group ◽  
Myocardial Ischemia Reperfusion

This study aimed to investigate the effects of miR-26a-5p and PTEN on myocardium of myocardial ischemia-reperfusion mice. Twelve C57/B6 male mice were randomly selected and divided into control group and mouse model group with 6 mice in each group, in which no surgical modeling was normally performed. Mice were killed 2 hours after operation to collect myocardial tissue. H9C2 was transfected with miR-26a-5p-mimic and blank vector to overexpress miR-26a-5p, and then normal group, hypoxia/reoxygenation group (cell model group), blank group and overexpression group were established respectively. Protein expressions of PTEN, Caspase-3, Caspase-9, P13K and p-Akt in tissues and cells of mice were detected. Expressions of miR-26a-5p and PTEN in myocardial tissue and cells of mice were detected. Apoptosis was detected. The relationship between miR-26a-5p and PTEN was determined. Expressions of miR-26a-5p in tissues of mouse model group were lower than those of normal group, while PTEN expressions were opposite (p<0.05). Expressions of miR-126 in overexpression group were increased compared with those of cell model group and blank group, and decreased compared with those of control group (P<0.05). Expressions of PTEN in overexpression group were lower than those in cell model group and blank group, and higher than those in control group (p<0.05). Compared with control group, miR-26a-5p was decreased and PTEN was increased in cell model group (P<0.05). Compared with blank group and cell model group, expressions of PTEN, Caspase-3 and Caspase-9 proteins in overexpression group were significantly decreased, while expressions of P13K and p-Akt proteins were significantly increased (p<0.05). Apoptosis rate in overexpression group was significantly lower than that in cell model group and blank group (p<0.05). Dual-luciferase reporter proved that there was a targeted regulatory relationship between miR-26a-5p and PTEN. In conclusion, up-regulation of miR-26a-5p regulates PTEN/PI3K/p-Akt signaling pathway and reduces myocardial cell apoptosis, thus improving ischemia-reperfusion injury.

Abstract 453: The Role of PD-1/PDL-1 in Myocardial Ischemia Reperfusion Injury.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mahmood Mozaffari ◽  
Jun Yao Liu ◽  
Babak Baban
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Inflammatory Response ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Interleukin 17 ◽  
Myocardial Ischemia Reperfusion

Programmed Death-1 (PD-1) and its ligand, PDL-1, are expressed on immune cells and have emerged as negative regulators of immune and inflammatory mechanisms. Aside from the contribution of systemic immune and inflammatory mechanisms to myocardial ischemia reperfusion (IR) injury, isolated heart studies have shown that the myocardium is capable of mounting a robust inflammatory response to an IR insult. However, potential involvement of PD-1/PDL-1 in the setting of cardiac IR injury is not established. We tested the hypothesis that an IR insult downregulates PD-1/PDL-1 pathway thereby exacerbating the inflammatory response and cell death. According, Langendorff-perfused rat hearts were subjected to 40 min of ischemia and 15 min of reperfusion; normoxic hearts served as controls. Thereafter, cardiac cells were prepared and subjected to flow-cytometry-based assays. The ischemic-reperfused hearts displayed a marked increase in the pro-inflammatory cytokine interleukin-17 in association with disruption of mitochondrial membrane potential (JC-1 assay) and apoptotic and necrotic cell death. Importantly, the ischemic-reperfused hearts showed a significant increase in PD-1 and PDL-1 positive cells. The results suggest that cardiac PD-1/ PDL-1 pathway likely constitutes an endogenous mechanism whose upregulation in the ischemic-reperfused heart curbs the inflammatory response and associated tissue injury.

scholarly journals The Protective Effect of Shuxin Shengmai Dan on Myocardial Ischemia-Reperfusion Injury in Rats

2020 ◽  
Author(s):  
Xingye Wang ◽  
Zhenzhu Hao ◽  
Xinghu Piao ◽  
Li Sun ◽  
Ye Tao ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Tissue ◽  
Tnf Α ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Abstract Background: The traditional Chinese medicine Shuxin Shengmai Dan (SXSMD) is clinically used to treat angina pectoris. The mechanism of action of SXSMD protection of the heart involves inhibition of inflammation and remains poorly understood. The role of SXSMD in rats with myocardial ischemia reperfusion (IR) and the mechanism of SXSMD action were studied in this research.Methods: The rats were treated with SXSMD (3.38, 6.76, and 13.52 g/kg/day, p.o.) or Danshen injecta (1.8 mL/kg/day, p.o.) for 15 days, then the coronary arteries were ligated. Cardiac function was evaluated by electrocardiography and hemodynamic measurements. Hematoxylin-eosin (H&E) staining was used to detect pathological changes in ischemic myocardial sections. Transmission electron microscopy (TEM) was used to assess the ultrastructure of cardiomyocytes. The changes in IL-6 and TNF-α in the rat serum were detected by ELISA. The changes in the expression levels of HMGB1, TLR4, MyD88, and NF-κB mRNAs and proteins related to the TLR4/NF-κB pathway in myocardial tissue were detected by qPCR and Western blot, respectively.Results: Rats with coronary artery ligation had abnormal cardiac function, inflammatory infiltration of myocardial cells, disordered myocardial fiber arrangement, accumulation of mitochondria, and disordered muscle fibers and sarcomeres according to electron microscopy. The levels of the expression of mRNAs and proteins in myocardial tissue of the SXSMD group were decreased compared with those in the MIRI group. The serum levels of IL-6 and TNF-α were decreased. SXSMD treatment can inhibit the inflammatory response and downregulate the TLR4/NF-κB pathway in cardiomyocytes.Conclusion: SXSMD protects the rats from myocardial ischemia-reperfusion injury in the MIRI model by downregulating the TLR4/NF-κB pathway to inhibit inflammation.

Mechanisms of cardioprotection by peroxynitrite in myocardial ischemia and reperfusion injury

1998 ◽  
Vol 275 (2) ◽  
pp. H509-H519 ◽  
Author(s):  
Tareck O. Nossuli ◽  
Reid Hayward ◽  
David Jensen ◽  
Rosario Scalia ◽  
Allan M. Lefer
Keyword(s):  
Myocardial Ischemia ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
No Donor ◽  
Myocardial Ischemia And Reperfusion ◽  
Rat Mesentery ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion ◽  
Feline Model

Peroxynitrite (ONOO−), an intermediate formed from the equimolar interaction of nitric oxide (NO) and superoxide, is thought to be an important mediator of tissue injury in myocardial ischemia-reperfusion. However, physiologically relevant (i.e., maximally achievable) concentrations of ONOO− significantly decreased neutrophil-endothelium interactions in the rat mesentery. We therefore examined the dose-response relationship of infusion of different concentrations of ONOO− in a feline model of myocardial ischemia-reperfusion and provide data on the cellular mechanisms responsible for these observed effects. Cats subjected to 90 min of ischemia followed by 270 min of reperfusion were infused with different concentrations of ONOO− 10 min before reperfusion and continuing throughout reperfusion. We observed that infusion of 2 μM ONOO−provided significant cardioprotection, whereas either 0.2 or 20 μM ONOO− did not protect. ONOO− at 2 μM also preserved coronary endothelial function, decreased P-selectin expression, and attenuated polymorphonuclear leukocyte (PMN) adherence to the vascular endothelium. ONOO− did not exert its cardioprotective effects by acting as a direct NO donor in solution. However, in vitro, ONOO− can react with glutathione to form S-nitrosoglutathione, which can act as an NO carrier and exert beneficial effects. Thus only maximally achievable concentrations of ONOO− exert significant cardioprotective effects, in part by decreasing surface expression of P-selectin and decreasing PMN-endothelium interactions.

scholarly journals The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Zhaoyan Xu ◽  
Yuanxi Mo ◽  
Xinyi Li ◽  
Wanzi Hong ◽  
Sisi Shao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Western Blot ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischemia Reperfusion ◽  
Myocardial Tissue ◽  
Qrt Pcr ◽  
Ischaemia Reperfusion ◽  
Myocardial Ischemia Reperfusion

Background: Myocardial ischaemia/reperfusion (I/R) injury is still a major challenge in clinical treatment. The role of long non-coding RNA (lncRNA) in the regulation of myocardial I/R injury still needs to be elucidated.Methods: The primary isolated neonatal mousse cardiomyocytes and adult mice were used to construct a myocardial ischemia-reperfusion model. qRT-PCR is used to verify gene expression in myocardial tissue and myocardial cells. The effect of AK035396 in primary cardiomyocytes and mouse myocardium was confirmed by TUNEL staining and in vitro flow cytometry experiments. RNA pulldown and Western blot were used to identify AK035396 interacting proteins. The expression of apoptosis-related proteins was identified by qRT-PCR and Western blot.Results:In vivo and in vitro MIRI models, AK035396 was up-regulated after myocardial infarction. Functional studies have shown that knockdown of AK035396 reduces the apoptosis of primary cardiomyocytes and mouse myocardial tissue. AK035396 directly interacts with Mterf1 and inhibits the level of Mterf1. Further experiments have shown that inhibiting Mterf1 will promote the expression of mitochondrial genes COXII and CYTb and cause cell apoptosis.Conclusion: AK035396 plays an important role in myocardial ischaemia-reperfusion injury by regulating the Mterf1-COXII/CYTb pathway.

scholarly journals Platelet-Activating Factor Acetylhydrolase Prevents Myocardial Ischemia-Reperfusion Injury

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Elizabeth N. Morgan ◽  
Edward M. Boyle ◽  
Wang Yun ◽  
John C. Kovacich ◽  
Timothy G. Canty ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Platelet Activating Factor ◽  
Neutrophil Infiltration ◽  
In Vivo Model ◽  
Area At Risk ◽  
Myocardial Ischemia Reperfusion

Background —Platelet-activating factor (PAF) is one of the most potent biological mediators of tissue injury. PAF acetylhydrolase (PAF-AH) is a recently isolated naturally occurring enzyme that hydrolyzes PAF and renders it inactive. We hypothesize that inhibition of PAF with PAF-AH will reduce myocardial ischemia-reperfusion (I/R) injury in vivo. Methods and Results —The coronary ligation model was used in New Zealand white rabbits. The large branch of the marginal coronary artery was occluded for 45 minutes, followed by 2 hours of reperfusion. Fifteen minutes before reperfusion, animals were given either 2 mg/kg of vehicle or of PAF-AH. At the completion of 120 minutes of reperfusion, percentage of necrosis, degree of neutrophil infiltration, and measurements of regional contractility were assessed. Data are expressed as the mean±SEM and compared by Student’s t test or Mann-Whitney ANOVA. Both groups of animals showed an equivalent area at risk; however, 46.7±11% was necrotic in the animal treated with vehicle. In contrast, 20.9±7.0% was necrotic in the animals treated with PAF-AH ( P <0.05). Systolic shortening and wall thickness were significantly greater in those animals treated with PAF-AH at 15, 30, 60, and 120 minutes of reperfusion ( P <0.05). Quantification of neutrophil infiltration showed a 62% reduction in the PAF-AH treated animals compared with those treated with vehicle alone. Conclusions —PAF-AH is a potent cardioprotective agent in an in vivo model of I/R injury.

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