Effective inhibition of cardiomyocyte apoptosis through the combination of trimetazidine and N-acetylcysteine in a rat model of myocardial ischemia and reperfusion injury

Şentürk, Tunay; Çavun, Sinan; Avcı, Berrin; Yermezler, Aysun; Serdar, Zehra Aşiran; Savci, Vahide

doi:10.1016/j.atherosclerosis.2014.10.091

Cited by 32 publications

(18 citation statements)

References 27 publications

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“…The MDA occurs naturally and is commonly used as a biomarker to measure the level of oxidative stress in an organism [18,19], especially in I/R injury in both myocardial [20] and skeletal muscles [21]. In this regard, the MDA was tested and the results showed ( Table 1) that, compared with sham, the amount of MDA was dramatically increased (4.94 ± 0.53 nM, P < 0.01) in the plasma of ischemic rats, which was further enhanced, at least double in amount, time-dependently following reperfusion in either I/R and saline-treated models and peaked at 8 h after I/R.…”

Section: Effects Of Msoda On Plasma Mda Before and After Ischemia/repmentioning

confidence: 99%

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

Wang¹,

Tian²,

Xu³

et al. 2015

Cell Physiol Biochem

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Background/Aim: Ischemia/reperfusion (I/R) injury of skeletal muscles is common pathophysiology during surgeries and the superoxide dismutase (SOD) plays a critical role in this process. SOD-modeled coordination compound (MSODa) may simulate the protective effects as SOD. Methods: Therefore, this study was designed to explore the protective effects and underlying mechanism of MSODa on malondialdehyde (MDA) and integrin-β2 (CD11b/CD18) in plasma, myeloperoxidase (MPO) and intercellular cell adhesion molecule-1 (ICAM-1) in tissue, and morphological changes before and after I/R injury. The rat model of I/R in hind limb was established and randomly divided into sham, ischemia, I/R, I/R-treated with saline, SOD, and MSODa, respectively. Results: These results showed that averaged values for MDA, MPO, CD11b/CD18, and ICAM-1 were significantly increased (P < 0.01 vs ischemia alone) in a time-dependent fashion along with marked tissue remodeling, such as abnormal arrangement of muscular fibers, interstitial edema, vasodilation with no-reflow, inflammatory cells adherent and infiltration, structural changes in mitochondrial, and decrease in glycogens as well. However, all parameter changes induced by I/R injury were reversed, at least partially, by MSODa and SOD treatments and intriguingly, the beneficial/protective effects of MSODa was superior to SOD with an early onset. Conclusion: This novel finding demonstrates that MSODa improves I/R injury of skeletal muscles due at least partially to inhibition of adherent molecule expression and reduction of oxygen free radical formation during I/R pathophysiological processes and this protective action of MSODa was superior to SOD, highlighting the bright future for MSODa in clinical management of tissue I/R injury.

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Section: Effects Of Msoda On Plasma Mda Before and After Ischemia/repmentioning

confidence: 99%

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

Wang¹,

Tian²,

Xu³

et al. 2015

Cell Physiol Biochem

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“…Although the foregoing findings indicate that adjunctive trimetazidine therapy is capable of reducing total MACE [20,21], there is conflicting evidence regarding trimetazidine's underlying effect upon infarcted myocardial tissue. For example, the work of Demirelli et al [22] on acute MI patients prescribed trimetazidine before and after PCI showed that adjunctive trimetazidine therapy was able to improve their myocardial performance index and left ventricular end-diastolic volume at the 30-day follow-up.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and Safety of Adjunctive Trimetazidine Therapy for Acute Myocardial Infarction: A Systematic Review and Meta-Analysis

Li¹,

Wang²,

Hu³

et al. 2016

Cardiology

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Background: Several lines of evidence support the clinical use of trimetazidine as an adjunctive therapy in cardioischemic patients. Therefore, we assessed here the efficacy and safety of adjunctive trimetazidine therapy in acute myocardial infarction (MI) patients by a systematic review and meta-analysis of the current literature. Methods: PubMed, the Cochrane Library, and the China National Knowledge Infrastructure databases were searched for clinical studies comparing adjunctive trimetazidine therapy against placebo in adult acute MI patients. Several clinical outcomes [early/short-term all-cause mortality, long-term all-cause mortality, total major adverse cardiac events (MACE), recurrent nonfatal MI, in-hospital adverse events, target vessel revascularization (TVR), and coronary artery bypass graft (CABG)] were analyzed by the intention-to-treat principle. Odds ratios (OR) and their 95% confidence intervals (CI) were derived from the number of outcome events in each study arm to estimate the association between adjuvant trimetazidine administration and the various clinical outcomes. A random-effects model was applied for all meta-analyses. Results: We found that adjunctive trimetazidine therapy showed a significant effect upon total MACE (OR = 0.33, 95% CI = 0.15-0.74; p = 0.007) but showed no significant effect upon early/short-term all-cause mortality, long-term all-cause mortality, recurrent nonfatal MI, in-hospital adverse events, TVR, or CABG (p > 0.05). Conclusions: This is the first meta-analysis to report that adjunctive trimetazidine therapy has a beneficial effect upon total MACE in acute MI patients. Clinical investigators should consider further trials on adjunctive trimetazidine therapy in order to better define its risks and benefits in acute MI patients.

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“…В эксперименте у крыс внутривенное введение три-метазидина приводило к существенному уменьшению зоны инфаркта, апоптоза кардиомиоцитов и показателей окислительного стресса [70]. В другом исследовании также отмечены возможности триметазидина в регуля-ции апоптоза кардиомиоцитов при повреждении мио-карда, вызванном ишемией и гипоксией [71].…”

Section: применение триметазидина позволяет сделать акцент при выбореunclassified

Myocardial Cytoprotector Trimetazidine Mb-Preparat, Increases the Effectiveness of Treatment of Chronic Heart Failure and Coronary Heart Disease

Трухан¹,

Давыдов²,

Мазуров³

2017

Med. sov.

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Effective inhibition of cardiomyocyte apoptosis through the combination of trimetazidine and N-acetylcysteine in a rat model of myocardial ischemia and reperfusion injury

Cited by 32 publications

References 27 publications

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

Protective Effects of Modeled Superoxide Dismutase Coordination Compound (MSODa) Against Ischemia/Reperfusion Injury in Rat Skeletal Muscle

Efficacy and Safety of Adjunctive Trimetazidine Therapy for Acute Myocardial Infarction: A Systematic Review and Meta-Analysis

Myocardial Cytoprotector Trimetazidine Mb-Preparat, Increases the Effectiveness of Treatment of Chronic Heart Failure and Coronary Heart Disease

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