scholarly journals Knock out hepatic Krüppel-like factor 16 (KLF16) improve myocardial damage and promoted myocardial protection of myocardial ischemia-reperfusion via anti-oxidative and anti-inflammation effects by TFAM/PPARβ signal passage

Bioengineered ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 10219-10231
Author(s):  
Yue Xin ◽  
Pixiong Su ◽  
Yan Liu ◽  
Song Gu ◽  
Xiangguang an ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Myocardial Protection ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Knock Out ◽  
Myocardial Ischemia Reperfusion ◽  
Signal Passage ◽  
Anti Inflammation

scholarly journals Membrane Attack Complex in Myocardial Ischemia/Reperfusion Injury: A Systematic Review for Post Mortem Applications

Diagnostics ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 898
Author(s):  
Cristina Mondello ◽  
Elvira Ventura Spagnolo ◽  
Luigi Cardia ◽  
Daniela Sapienza ◽  
Serena Scurria ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Membrane Attack Complex ◽  
Myocardial Damage ◽  
Post Mortem ◽  
Complement Components ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

The complement system has a significant role in myocardial ischemia/reperfusion injury, being responsible for cell lysis and amplification of inflammatory response. In this context, several studies highlight that terminal complement complex C5b-9, also known as the membrane attack complex (MAC), is a significant contributor. The MAC functions were studied by many researchers analyzing the characteristics of its activation in myocardial infarction. Here, a systematic literature review was reported to evaluate the principal features, advantages, and limits (regarding the application) of complement components and MAC in post mortem settings to perform the diagnosis of myocardial ischemia/infarction. The review was performed according to specific inclusion and exclusion criteria, and a total of 26 studies were identified. Several methods studied MAC, and each study contributes to defining better how and when it affects the myocardial damage in ischemic/reperfusion injury. The articles were discussed, focusing on the specificity, sensibility, and post mortem stability of MAC as a marker of myocardial ischemia/infarction, supporting the usefulness in routine post mortem investigations.

scholarly journals On the significance of hyperlactatemia in the implementation of the infarct-limiting effect of remote ischemic postconditioning in myocardial ischemia-reperfusion in the experiment

2020 ◽  
Vol 64 (3) ◽  
pp. 332-340
Author(s):  
S. N. Chepelev ◽  
F. I. Vismont ◽  
S. V. Goubkin
Keyword(s):  
Myocardial Ischemia ◽  
Clinical Medicine ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Modern Medicine ◽  
Ischemic Postconditioning ◽  
Social Significance ◽  
Remote Ischemic Postconditioning ◽  
Urgent Task ◽  
Myocardial Ischemia Reperfusion

Modern medicine faces the problem of the growth of cardiovascular pathology. Given the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods to prevent or weaken ischemic myocardial damage and mechanisms for their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to determine the significance of hyperlactatemia in the realization of the infarct-limiting effect of remote ischemic postconditioning (RIPostC) in rat myocardial ischemia-reperfusion in the experiment. The study revealed that after 15-minute RIPostC, which was performed 10 minutes after 30-minute acute myocardial ischemia followed by 120-minute reperfusion, the plasma lactate level in rats increased 1.87 times (87.7 %, p < 0.05) compared with intact animals. It was established that the introduction of L-lactate into the left common jugular vein at a dose of 10 μg/kg, which was carried out 25 minutes after the onset of reperfusion under the conditions of myocardial ischemia (30 minutes) and next reperfusion (120 minutes) and RIPostC (10 minutes after the onset of reperfusion), which was reproduced by ischemia of these limbs, have a heart attack-limiting effect. The increase of the level of blood lactate (hyperlactatemia) after RIPostC in myocardial ischemia-reperfusion is of significance in the implementation of its infarct-limiting effect.

A functional polysaccharide from Eriobotrya japonica relieves myocardial ischemia injury via anti-oxidation and anti-inflammation

2021 ◽  
Author(s):  
Xiaoli Huang ◽  
Ranran Hou ◽  
Wei Pan ◽  
Dingtao Wu ◽  
Wenwen Zhao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Eriobotrya Japonica ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Anti Inflammation

We herein report a food-derived polysaccharide (EJP) with the effect of relieving myocardial ischemia reperfusion injury (MIRI). This novel polysaccharide was isolated from the leaf of Eriobotrya japonica, and we...

scholarly journals Downregulated LINC01614 Ameliorates Hypoxia/Reoxygenation-Stimulated Myocardial Injury by Directly Sponging microRNA-138-5p

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091378 ◽  
Author(s):  
Jie Yang ◽  
Xue-Song Yang ◽  
Qian Zhang ◽  
Xin Zhuang ◽  
Xiao-Kang Dong ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Gene Expression Omnibus ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Myocardial Ischemia Reperfusion ◽  
Dual Luciferase Reporter Assay ◽  
Hypoxia Reoxygenation

Background: LINC01614 was abnormally expressed in myocardial infarction and other heart failures. We attempted to detect the effects of LINC01614 in myocardial ischemia–reperfusion (I/R) injury. Methods: H9c2 cardiomyocyte cells were treated with hypoxia/reoxygenation (H/R) to establish myocardial ischemia (MI) model. Results: Clinical data of Gene Expression Omnibus (GEO) database indicated that LINC01614 was highly regulated in first acute myocardial infarction, whereas miR-138-5p was downregulated in unstable angina pectoris. LINC01614 inhibition promoted cell proliferation and repressed the apoptotic property after H/R treatment using Cell Counting Kit-8 and flow cytometry analysis. Downregulation of LINC01614 enhanced the expression of Bcl-2 but attenuated Bax and cleaved caspase 3 expression after H/R treatment. Bioinformatics prediction and dual-luciferase reporter assay determined that LINC01614 directly targeted miR-138-5p and negatively regulated the expression of miR-138-5p. Furthermore, the overexpression of miR-138-5p significantly strengthened the function of si-LINC01614 in H/R groups. Conclusion: Our results illustrated that reduction in LINC01614 attenuated H/R treatment-induced myocardial damage via sponging miR-138-5p.

scholarly journals Poly(I:C) preconditioning protects the heart against myocardial ischemia/reperfusion injury through TLR3/PI3K/Akt-dependent pathway

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Erya Chen ◽  
Chan Chen ◽  
Zhendong Niu ◽  
Lu Gan ◽  
Qiao Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Poly I:C ◽  
Knock Out ◽  
Polycytidylic Acid ◽  
Myocardial Ischemia Reperfusion

Abstract Emerging evidence suggests that Toll-like receptors (TLRs) ligands pretreatment may play a vital role in the progress of myocardial ischemia/reperfusion (I/R) injury. As the ligand of TLR3, polyinosinic-polycytidylic acid (poly(I:C)), a synthetic double-stranded RNA, whether its preconditioning can exhibit a cardioprotective phenotype remains unknown. Here, we report the protective effect of poly(I:C) pretreatment in acute myocardial I/R injury by activating TLR3/PI3K/Akt signaling pathway. Poly(I:C) pretreatment leads to a significant reduction of infarct size, improvement of cardiac function, and downregulation of inflammatory cytokines and apoptotic molecules compared with controls. Subsequently, our data demonstrate that phosphorylation of TLR3 tyrosine residue and its interaction with PI3K is enhanced, and protein levels of phospho-PI3K and phospho-Akt are both increased after poly(I:C) pretreatment, while knock out of TLR3 suppresses the cardioprotection of poly(I:C) preconditioning through a decreased activation of PI3K/Akt signaling. Moreover, inhibition of p85 PI3K by the administration of LY294002 in vivo and knockdown of Akt by siRNA in vitro significantly abolish poly(I:C) preconditioning-induced cardioprotective effect. In conclusion, our results reveal that poly(I:C) preconditioning exhibits essential protection in myocardial I/R injury via its modulation of TLR3, and the downstream PI3K/Akt signaling, which may provide a potential pharmacologic target for perioperative cardioprotection.

Abstract 350: Toll-like Receptor 2 Activation, Especially In Circulating Leukocytes, Mediates Myocardial Ischemia/Reperfusion Injury In Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Fatih Arslan ◽  
Gerard Pasterkamp ◽  
Leo Timmers ◽  
Ben van Middelaar ◽  
Pieter A Doevendans ◽  
...  
Keyword(s):  
At Risk ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Blue Dye ◽  
Tlr2 Expression ◽  
Area At Risk ◽  
Saline Treatment ◽  
Myocardial Ischemia Reperfusion

OBJECTIVES. Myocardial ischemia/reperfusion (MI/R) injury is characterized by an inflammatory response through NF-κB, increase of infarct size and worsening of cardiac function. Toll-like receptors (TLRs) are part of innate immunity and initiate the same inflammatory reaction. Here we studied in vivo to what extent TLR2 is involved in myocardial damage and what the relative contribution is of TLR2 expression in parenchymal cells and leukocytes to myocardial damage during MI/R in mice. METHODS. C57Bl6J mice underwent 30 minutes ischemia - 24 hours of reperfusion. Four experimental groups were studied: TLR2 knock-out (TLR2 KO) mice (n=10), saline treated wild-type (WT) mice (n=10), generated chimeric WT mice with TLR2 KO bone marrow (BLOOD KO; n=7) and chimeric TLR2 KO mice with WT hematopoietic cells (ORGAN KO; n=7). Saline was administered via the tail vein 5 minutes prior to reperfusion. After 24 hours, the LCA was ligated again at the level marked by the suture left in place. Mice were terminated and infarct size (IS) was measured as a percentage of the area at risk (AAR) using 4% Evans’ blue dye injection in the aortic root and triphenyltetrazolium chloride (TTC) staining (fig. 1). Data are presented as Mean±SEM. RESULTS. The AAR as percentage of the left ventricle was similar between groups: TLR2 KO 41%, saline 41%, Blood KO 41%, Organ KO 42%. Saline treatment resulted in 34.5%±3.3 of infarction, whereas in TLR2 KO mice infarct size decreased to 23.0%±2.9 (p=0.029 vs. saline). Infarct size in BLOOD KO mice was 22.9%±2.7 (p=0.024 vs. saline), while ORGAN KO mice had 33.9%±3.2 (p=0.998 vs. saline) of infarction within the area at risk (fig. 2). CONCLUSION. TLR2 deficiency significantly reduces infarct size with ~33% compared to saline treatment in mice after 30 minutes of ischemia and 24 hours of reperfusion. We show for the first time that TLR2 expression in circulating leukocytes plays an important role in infarction after MI/R injury. Systemic inhibition of TLR2 may be a potential therapeutic target in the treatment of patients with acute myocardial infarction.

Neohesperidin alleviated pathological damage and immunological imbalance in rat myocardial ischemia-reperfusion injury via inactivation of JNK and NF-κB p65

2021 ◽  
Vol 85 (2) ◽  
pp. 251-261
Author(s):  
Aihua Li ◽  
Xin Zhang ◽  
Qiuping Luo
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Inflammatory Cytokines ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Oxidative Stress Markers ◽  
Antitumor Effects ◽  
Stress Markers ◽  
Myocardial Ischemia Reperfusion

ABSTRACT Neohesperidin (NEO) exerts antiviral, antioxidant, anti-inflammation, and antitumor effects in some diseases. The purpose of this study was to investigate the effect and mechanism of NEO on myocardial ischemia-reperfusion (I/R) injury. Results indicated that NEO suppressed the levels of serum inflammatory cytokines, myocardial damage markers, and oxidative stress markers, and increased the levels of antioxidant in myocardial I/R rats. NEO also inhibited cell apoptosis. Besides, NEO also inhibited the phosphorylation of c-Jun N-terminal kinases (JNK) and nuclear factor kappa B (NF-κB) p65. Furthermore, the protective effects of NEO on myocardial tissue damage, inflammatory cytokines, myocardial injury markers, oxidative stress markers, cell apoptosis, spleen, thymus and liver indices, and phagocytic indices were reversed by JNK activator and NF-κB activator, respectively. In conclusion, NEO alleviates myocardial damage, oxidative stress, cell apoptosis, and immunological imbalance in I/R injury via the inactivation of JNK and NF-κB, making NEO a potential agent for myocardial I/R therapy.

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