Inflammation, Proinflammatory Mediators and Myocardial Ischemia–reperfusion Injury

Vinten‐Johansen, Jakob; Jiang, Rong; Reeves, James G.; Mykytenko, James; Deneve, Jeremiah; Jobe, Lynetta J.

doi:10.1016/j.hoc.2006.11.010

Cited by 74 publications

(55 citation statements)

References 129 publications

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“…The inflammatory response is stimulated by I/R injury, leading to the release of inflammatory cytokines, which are critical mediators of infarct healing and cardiac remodeling [31]. In addition, inhibiting inflammation can decrease myocardial I/R injury and preserve cardiac function [32, 33].…”

Section: Discussionmentioning

confidence: 99%

Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

Shu

Zhang

Huang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Troxerutin, also known as vitamin P4, has been commonly used in the treatment of chronic venous insufficiency (CVI) disease. However, its effect on in vivo myocardial ischemia/reperfusion (I/R) injury, a model that closely mimics acute myocardial infarction in humans, is still unknown. Methods: The myocardial I/R injury rat model was created with troxerutin preconditioning. Myocardial infarct size was evaluated by the Evans blue-TTC method. Hemodynamic parameters, including the heart rate (HR), left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximal rate of rise in blood pressure in the ventricular chamber (+dp/dt max), and maximal rate of decline in blood pressure in the ventricular chamber (-dp/dt max) were monitored. Serum TNF-α and IL-10 were determined by ELISA kit. Cell apoptosis was detected by MTT method. Results: Troxerutin preconditioning significantly reduced myocardial infarct size, improved cardiac function, and decreased the levels of creatine kinase (CK), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the I/R injury rat model. The serum and mRNA levels of TNF-α and IL-10 as well as some apoptosis markers (Bax, Caspase 3) also decreased. Moreover, troxerutin pretreatment markedly increased the phosphorylation of Akt, and blocking PI3K activity by LY294002 abolished the protective effect of troxerutin on I/R injury. Conclusion: Troxerutin preconditioning protected against myocardial I/R injury via the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

Shu

Zhang

Huang

et al. 2017

Cell Physiol Biochem

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“…Inflammation is one of the important factors which results in ventricular dysfunction following IRI and the expression of inflammatory cytokines and the deterioration of myocardial function is highly correlated [26]. Inflammation will stimulate many factors to aggravate the myocardial function [27].…”

Section: Discussionmentioning

confidence: 99%

Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model

Chen

Huang

et al. 2012

Inflammation

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In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following cardiac arrest (CA) in a rabbit model. Lipoxin A4 is a metabolite of arachidonic acid in the eicosanoid, it is called "brake signal" for its anti-inflammatory activity. Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. Lipoxin A4 inhibits the expression of IL-1β, IL-6, and TNF-α, the values of the infarct ratios, apoptotic index, the level of serum cTnI and NF-κB p65. Meanwhile, it improves the expression of IL-10, hemodynamic, myocardial structure, and function. These indicate that lipoxin A4 mitigates postresuscitation myocardial IRI in which anti-inflammation and suppression of NF-κB activation may play an important role.

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“…However, the vascular endothelium is also spared by postconditioning. It is the opinion of the authors and other investigators that the coronary vascular endothelium is a critical factor in the initiation of the inflammatory response to reperfusion, and as such preservation of Table 1 Events that occur during the early moments of reperfusion the coronary vascular endothelium is causally related to a reduction in infarct size, as has been reviewed elsewhere [33][34][35][36]. The remainder of the review will discuss the mechanisms by which postconditioning reduces necrosis and apoptosis.…”

Section: Protection Against Acute Myocardial Infarctionmentioning

confidence: 99%

Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion

Vinten‐Johansen

2007

Heart Fail Rev

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Infarct size is determined not only by the duration and severity of ischemia, but also by pathological processes initiated at reperfusion (reperfusion injury). Numerous pharmacological strategies have been reported which administer drugs at or just before the onset of reperfusion, with subsequent salubrious effects, notably a reduction in infarct size. However, few if any of these strategies have become standard of care in the catheterization laboratory setting. Postconditioning, defined as repeated brief cycles of reperfusion interrupted by ischemia (or hypoxia) applied at the onset of reperfusion, was recently introduced as a mechanical strategy to attenuate reperfusion injury. Postconditioning intervenes only during the first few minutes of reperfusion. However, it reduces endothelial activation and dysfunction, the inflammatory response to reperfusion, necrosis, and apoptosis both acutely and long-term. Cardioprotection has been demonstrated by multiple independent laboratories and in multiple species. Postconditioning stimulates G-protein coupled receptors by their cognate endogenously released ligands and surprisingly activates survival kinases that may converge on mitochondrial K(ATP) channels and the permeability transition pore. Postconditioning has been shown in two clinical studies to reduce infarct size in patients undergoing percutaneous coronary intervention in the catheterization laboratory, and at least five other studies are in some phase of implementation. This significant reduction in infarct size has implications for reduction in heart failure as a consequence of myocardial infarction, but this link has yet to be demonstrated. The salubrious effects of postconditioning are an indirect validation of the experimental and clinical importance of reperfusion injury in the setting of coronary artery occlusion.

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Inflammation, Proinflammatory Mediators and Myocardial Ischemia–reperfusion Injury

Cited by 74 publications

References 129 publications

Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

Effect of Lipoxin A4 on Myocardial Ischemia Reperfusion Injury Following Cardiac Arrest in a Rabbit Model

Postconditioning: a mechanical maneuver that triggers biological and molecular cardioprotective responses to reperfusion

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