scholarly journals Inactivated Lactobacillus promotes protection against myocardial ischemia–reperfusion injury through NF-κB pathway

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Ni Wang ◽  
Genhong Song ◽  
Yang Yang ◽  
Weiwei Yuan ◽  
Ming Qi
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Group Model ◽  
Content Increase ◽  
Model Group ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content ◽  
Myocardial Ischemia Reperfusion

Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion may augment tissue injury in excess of that produced by ischemia alone. So this experiment was designed to study the protective effects and mechanism of inactivated Lactobacillus (Lac) on myocardial ischemia–reperfusion (I–R) injury (MIRI). MIRI rat models were established by ligation of left anterior descending coronary artery for ~30 min and then, reperfusion for 120 min and divided into control group, model group, and Lac (106, 107, and 108 cfu/kg) groups. At the end of the test, the creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assayed by corresponding kits. The heart was obtained from rats and the myocardial infarction area was determined by TTC staining and myocardial endothelial cell apoptosis rate was determined by Tunel kit. Besides, A20, IκB, nuclear factor (NF)-κB, and nitric oxide (NO) synthase (NOS) were also assayed by Western blot. When compared with model group, Lac obviously reduces MIRI in the rat by reducing myocardial infarction area and the apoptosis rate of endothelial cells; reduce the serum CK, LDH, and MDA content; increase the serum SOD activity; and suppress NF-κB signaling and NOS expression in the myocardial tissues. Lac pretreatment can inhibit lipid peroxidation and effectively improve MIRI caused by oxygen free radical through inhibiting NF-κB signaling.

scholarly journals Trop2 Guarantees Cardioprotective Effects of Cortical Bone-Derived Stem Cells on Myocardial Ischemia/Reperfusion Injury

2018 ◽  
Vol 27 (8) ◽  
pp. 1256-1268 ◽  
Author(s):  
Tianyu Li ◽  
Yunshu Su ◽  
Xiongli Yu ◽  
Durgahee S.A. Mouniir ◽  
Jackson Ferdinand Masau ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Myocardial Ischemia ◽  
Cortical Bone ◽  
Heart Function ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Promising Therapeutic Approach ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion

Stem cell transplantation represents a promising therapeutic approach for myocardial ischemia/reperfusion (I/R) injury, where cortical bone-derived stem cells (CBSCs) stand out and hold superior cardioprotective effects on myocardial infarction than other types of stem cells. However, the molecular mechanism underlying CBSCs function on myocardial I/R injury is poorly understood. In a previous study, we reported that Trop2 (trophoblast cell-surface antigen 2) is expressed exclusively on the CBSCs membrane, and is involved in regulation of proliferation and differentiation of CBSCs. In this study, we found that the Trop2 is essential for the ameliorative effects of CBSCs on myocardial I/R-induced heart damage via promoting angiogenesis and inhibiting cardiomyocytes apoptosis in a paracrine manner. Trop2 is required for the colonization of CBSCs in recipient hearts. When Trop2 was knocked out, CBSCs largely lost their functions in lowering myocardial infarction size, improving heart function, enhancing capillary density, and suppressing myocardial cell death. Mechanistically, activating the AKT/GSK3β/β-Catenin signaling axis contributes to the essential role of Trop2 in CBSCs-rendered cardioprotective effects on myocardial I/R injury. In conclusion, maintaining the expression and/or activation of Trop2 in CBSCs might be a promising strategy for treating myocardial infarction, I/R injury, and other related heart diseases.

scholarly journals Ischemia/Reperfusion Injury: Pathophysiology, Current Clinical Management, and Potential Preventive Approaches

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
César Daniel Sánchez-Hernández ◽  
Lucero Aidé Torres-Alarcón ◽  
Ariadna González-Cortés ◽  
Alberto N. Peón
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Inflammatory Mediators ◽  
Clinical Management ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mechanisms Of Action ◽  
Myocardial Ischemia Reperfusion ◽  
Experimental Treatments ◽  
The Many

Myocardial ischemia reperfusion syndrome is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. In such a setting, the establishment of an effective therapy to treat this condition has been elusive, perhaps because the experimental treatments have been conceived to block just one of the many pathogenic pathways of the disease, or because they thwart the tissue-repairing phase of the syndrome. Either way, we think that a discussion about the pathophysiology of the disease and the mechanisms of action of some drugs may shed some clarity on the topic.

scholarly journals Ginsenoside Rb1 for Myocardial Ischemia/Reperfusion Injury: Preclinical Evidence and Possible Mechanisms

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Qun Zheng ◽  
Xiao-Yi Bao ◽  
Peng-Chong Zhu ◽  
Qiang Tong ◽  
Guo-Qing Zheng ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Creatine Kinase ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ginsenoside Rb1 ◽  
Creatine Kinase Mb ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Ginseng is an important herbal drug that has been used worldwide for many years. Ginsenoside Rb1 (G-Rb1), the major pharmacological extract from ginseng, possesses a variety of biological activities in the cardiovascular systems. Here, we conducted a preclinical systematic review to investigate the efficacy of G-Rb1 for animal models of myocardial ischemia/reperfusion injury and its possible mechanisms. Ten studies involving 211 animals were identified by searching 6 databases from inception to May 2017. The methodological quality was assessed by using the CAMARADES 10-item checklist. All the data were analyzed using RevMan 5.3 software. As a result, the score of study quality ranged from 3 to 7 points. Meta-analyses showed that G-Rb1 can significantly decrease the myocardial infarct size and cardiac enzymes (including lactate dehydrogenase, creatine kinase, and creatine kinase-MB) when compared with control group (P<0.01). Significant decrease in cardiac troponin T and improvement in the degree of ST-segment depression were reported in one study (P<0.05). Additionally, the possible mechanisms of G-Rb1 for myocardial infarction are antioxidant, anti-inflammatory, antiapoptosis, promoting angiogenesis and improving the circulation. Thus, G-Rb1 is a potential cardioprotective candidate for further clinical trials of myocardial infarction.

scholarly journals Protective Effect of Shexiang Baoxin Pill on Myocardial Ischemia/Reperfusion Injury in Patients With STEMI

2021 ◽  
Vol 12 ◽  
Author(s):  
Haixia Qin ◽  
Siyuan Li ◽  
Zhenbing Liu
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
St Segment ◽  
Myocardial Ischemia Reperfusion ◽  
Shexiang Baoxin Pill ◽  
Peak Value

Background: There is no definite effect in the treatment of myocardial ischemia/reperfusion (I/R) injury in patients with acute ST-segment elevation myocardial infarction (STEMI). We evaluated the protective effect of Shexiang Baoxin Pill (SBP) on I/R injury in STEMI patients.Methods: STEMI patients were randomly divided into a primary percutaneous coronary intervention (PPCI) group (n = 52) and a PPCI + SBP group (n = 51). The area at risk of infarction (AAR) and final infarct size (FIS) were examined by single-photon emission computed tomography (SPECT). I/R injury was assessed using myocardial salvage (MS) and salvage index (SI) calculated from AAR and FIS.Results: The ST-segment resolution (STR) in the PPCI + SBP group was significantly higher than that in the PPCI group (p = 0.036), and the peak value of high-sensitivity troponin T (hsTNT) was lower than that in the PPCI group (p = 0.048). FIS in the PPCI + SBP group was smaller than that in the PPCI group (p = 0.047). MS (p = 0.023) and SI (p = 0.006) in the PPCI + SBP group were larger than those in the PPCI group. The left ventricular ejection fraction (LVEF) in the PPCI + SBP group was higher than that in the PPCI group (p = 0.049), and N-terminal pro-B type natriuretic peptide (NT-proBNP) level in the PPCI + SBP group was lower than that in the PPCI group (p = 0.048).Conclusions: SBP can alleviate I/R injury (MS and SI), decrease myocardial infarction area (peak value of hsTNT and FIS), and improve myocardial reperfusion (MBG and STR) and cardiac function (LVEF and NT-proBNP).

scholarly journals AMPK/SIRT1 Pathway is Involved in Arctigenin-Mediated Protective Effects Against Myocardial Ischemia-Reperfusion Injury

2021 ◽  
Vol 11 ◽  
Author(s):  
Cheng-Yin Liu ◽  
Yi Zhou ◽  
Tao Chen ◽  
Jing-Chao Lei ◽  
Xue-Jun Jiang
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Dependent Manner ◽  
Protective Effects ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Arctigenin, one of the active ingredients extracted from Great Burdock (Arctium lappa) Achene, has been found to relieve myocardial infarction injury. However, the specific mechanism of Arctigenin against myocardial infarction remains largely unknown. Here, both acute myocardial ischemia-reperfusion injury (AMI/R) rat model and oxygen glucose deprivation (OGD)-induced myocardial cell injury model were constructed to explore the underlying role of AMPK/SIRT1 pathway in Arctigenin-mediated effects. The experimental data in our study demonstrated that Arctigenin ameliorated OGD-mediated cardiomyocytes apoptosis, inflammation and oxidative stress in a dose-dependent manner. Besides, Arctigenin activated AMPK/SIRT1 pathway and downregulated NF-κB phosphorylation in OGD-treated cardiomyocytes, while inhibiting AMPK or SIRT1 by the Compound C (an AMPK inhibitor) or SIRT1-IN-1 (a SIRT1 inhibitor) significantly attenuated Arctigenin-exerted protective effects on cardiomyocytes. In the animal experiments, Arctigenin improved the heart functions and decreased infarct size of the AMI/R-rats, accompanied with downregulated oxidative stress, inflammation and apoptotic levels in the heart tissues. What’s more, Arctigenin enhanced the AMPK/SIRT1 pathway and repressed NF-κB pathway activation. Taken together, our data indicated that Arctigenin reduced cardiomyocytes apoptosis against AMI/R-induced oxidative stress and inflammation at least via AMPK/SIRT1 pathway.

scholarly journals The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2134
Author(s):  
Alessandro Bellis ◽  
Ciro Mauro ◽  
Emanuele Barbato ◽  
Giuseppe Di Gioia ◽  
Daniela Sorriento ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Systolic Function ◽  
Ischemia Reperfusion ◽  
St Elevation Myocardial Infarction ◽  
St Elevation ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

During the last three decades, timely myocardial reperfusion using either thrombolytic therapy or primary percutaneous intervention (pPCI) has allowed amazing improvements in outcomes with a more than halving in 1-year ST-elevation myocardial infarction (STEMI) mortality. However, mortality and left ventricle (LV) remodeling remain substantial in these patients. As such, novel therapeutic interventions are required to reduce myocardial infarction size, preserve LV systolic function, and improve survival in reperfused-STEMI patients. Myocardial ischemia-reperfusion injury (MIRI) prevention represents the main goal to reach in order to reduce STEMI mortality. There is currently no effective therapy for MIRI prevention in STEMI patients. A significant reason for the weak and inconsistent results obtained in this field may be the presence of multiple, partially redundant, mechanisms of cell death during ischemia-reperfusion, whose relative importance may depend on the conditions. Therefore, it is always more recognized that it is important to consider a “multi-targeted cardioprotective therapy”, defined as an additive or synergistic cardioprotective agents or interventions directed to distinct targets with different timing of application (before, during, or after pPCI). Given that some neprilysin (NEP) substrates (natriuretic peptides, angiotensin II, bradykinin, apelins, substance P, and adrenomedullin) exert a cardioprotective effect against ischemia-reperfusion injury, it is conceivable that antagonism of proteolytic activity by this enzyme may be considered in a multi-targeted strategy for MIRI prevention. In this review, by starting from main pathophysiological mechanisms promoting MIRI, we discuss cardioprotective effects of NEP substrates and the potential benefit of NEP pharmacological inhibition in MIRI prevention.

scholarly journals Effects on cardiac function, remodeling and inflammation following myocardial ischemia–reperfusion injury or unreperfused myocardial infarction in hypercholesterolemic APOE*3-Leiden mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Niek J. Pluijmert ◽  
Cindy I. Bart ◽  
Wilhelmina H. Bax ◽  
Paul H. A. Quax ◽  
Douwe E. Atsma
Keyword(s):  
Myocardial Infarction ◽  
Clinical Trials ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Apo E ◽  
Lv Remodeling ◽  
Myocardial Ischemia Reperfusion

Abstract Many novel therapies to treat myocardial infarction (MI), yielding promising results in animal models, nowadays failed in clinical trials for several reasons. The most used animal MI model is based on permanent ligation of the left anterior descending (LAD) coronary artery in healthy mice resulting in transmural MI, while in clinical practice reperfusion is usually accomplished by primary percutaneous coronary interventions (PCI) limiting myocardial damage and inducing myocardial ischemia–reperfusion (MI-R) injury. To evaluate a more similar murine MI model we compared MI-R injury to unreperfused MI in hypercholesterolemic apolipoprotein (APO)E*3-Leiden mice regarding effects on cardiac function, left ventricular (LV) remodeling and inflammation. Both MI-R and MI resulted in significant LV dilation and impaired cardiac function after 3 weeks. Although LV dilation, displayed by end-diastolic (EDV) and end-systolic volumes (ESV), and infarct size (IS) were restricted following MI-R compared to MI (respectively by 27.6% for EDV, 39.5% ESV, 36.0% IS), cardiac function was not preserved. LV-wall thinning was limited with non-transmural LV fibrosis in the MI-R group (66.7%). Two days after inducing myocardial ischemia, local leucocyte infiltration in the infarct area was decreased following MI-R compared to MI (36.6%), whereas systemic circulating monocytes were increased in both groups compared to sham (130.0% following MI-R and 120.0% after MI). Both MI-R and MI models against the background of a hypercholesterolemic phenotype appear validated experimental models, however reduced infarct size, restricted LV remodeling as well as a different distributed inflammatory response following MI-R resemble the contemporary clinical outcome regarding primary PCI more accurately which potentially provides better predictive value of experimental therapies in successive clinical trials.

Effect of Vaspin on Myocardial Ischemia-Reperfusion Injury Rats and Expression of NLR Family Pyrin Domain Containing 3 (NLRP3)

2020 ◽  
Vol 10 (6) ◽  
pp. 895-900 ◽  
Author(s):  
Lili Xu ◽  
Zhe Wang ◽  
Lixiang Deng
Keyword(s):  
Myocardial Ischemia ◽  
Type I Collagen ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Type I ◽  
Sod Activity ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Nlrp3 Expression

Myocardial ischemia-reperfusion injury (MIRI) can cause myocardial damage. Vaspin can protect against myocardial damage. However, the effect of vaspin on MIRI rats and the expression of NLRP3 remains unclear. Sprague-Dawley rats were separated into sham group; MIRI group and Vaspin group, in which 100 ng/ml vaspin was administrated before model preparation followed by analysis of cardiac function by M-mode ultrasound, level of NLRP3, of type I collagen, IL-6 and TNF-α by ELISA, SOD activity and ROS by spectrophotometry and Bcl-2 and PI3K/AKT signaling protein expression by Western Blot. In MIRI group, left ventricular end-systolic diameter (LVESD), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), NLRP3 expression, contents of type I collagen, IL-6, TNF-α as well as ROS were significantly increased and SOD activity was significantly decreased with decreased Bcl-2 expression and upregulated pAKT and pPI3K (P < 0.05). In Vaspin group, LVESD, LVMI and LVEDD and NLRP3 expression as well as type I collagen, IL-6, TNF-α and ROS was decreased, SOD activity and Bcl-2 expression was significantly increased with downregulated pAKT and pPI3K (P < 0.05). Vaspin can regulate PI3K/AKT signaling pathway, inhibit NLRP3 expression, regulate oxidative stress, inhibit inflammation, reduce apoptosis, improve and improve cardiac function of myocardial ischemia-reperfusion injury in rats.

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