The Effect of Hepcidin on Cardiac Ischemia-Reperfusion Injury

Bayraktar, Atilla; Erbaş, Deniz; Dizakar, Saadet Özen Akarca; Goktas, Guleser; Ömeroğlu, Suna; Oyar, Eser Oz

doi:10.1080/08941939.2019.1579275

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…Unfortunately, cardiomyocyte is a nonrenewable tissue and cell apoptosis will terminate with DNA damage and cell death. 24,25 This was evaluated in our study that detected significant increase of the active cas-pase3 and TNF-α levels in DOX given group but VIN treated groups showed significant decrease of the measured inflammatory and apoptotic agents that could be supported by other studies. 8,23,26 Despite extensive research on the mechanisms of DOX cardiotoxicity, the pathogenesis is still unclearly understood.…”

Section: Discussionsupporting

confidence: 79%

“…This is in accordance with different previous studies. 25,28 Based on the critical role of cAMP/cGMP/SIRT pathway, PDE inhibition is mandatory to keep the myocardium, protect blood vessels and preserve the tissue. It plays an essential role in regulating apoptosis, resisting oxidative stress, alleviating inflammation and protecting the mitochondrial function.…”

Section: Discussionmentioning

confidence: 99%

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Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity via modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways

et al. 2022

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Purpose: Doxorubicin (DOX) is a widely used chemotherapeutic agent complicated with cardiotoxic adverse effects. Up till now, there are no researches discussing the role of vinpocetine (VIN) in DOX cardiotoxicity. Thus, the aim of our work was to study this effect and explore the different involved mechanisms. Methods: 50 male Wistar albino rats were subjected to DOX toxicity via administration of single i.p. Dose (15 mg/kg) on the 4th day with or without co-administration of VIN (10, 20, 30 mg/kg/day) orally for 5 days. Results: Our data revealed that VIN succeeded in protecting the heart against DOX induced damage as manifested by significant decrease of cardiac enzymes, hypoxia inducible factor alpha (HIF-1α), vascular endothelial growth factor-A (VEGF-A), tissue malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α) and caspase3 levels. Furthermore, VIN given group showed marked improvement of the histopathological changes of cardiac injury, total antioxidant capacity (TAC), elevation of reduced glutathione (GSH), cyclic guanosine monophosphate (cGMP), cyclic adenosine monophosphate (cAMP) and sirtuin-1 (SIRT-1). Conclusion: We concluded that VIN could ameliorate DOX induced cardiac damage and this effect may be attributed to modulation of HIF/VEGF signaling pathway, up-regulation of cGMP/cAMP/SIRT pathway, inhibition of phosphodiesterase enzyme, besides its anti-apoptotic, anti-inflammatory, and anti-oxidant properties.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity via modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways

et al. 2022

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“…The animals were heparinized and anesthetized with a freshly prepared ketamine HCL administrated intraperitoneally at a dose of 60 mg/kg. 15 After stabilization, the rat was placed supine on the surgical table. The hearts were detached and instantly submerged in ice-cold Krebs–Henseleit buffer containing 11.1 mM of glucose, 118 mM of NaCl, 1.5 mM of CaCl 2 , 25.2 mM of NaHCO 3 , 4.7 mM of KCl, 1.2 mM of MgSO 4 , and 1.2 mM of KH 2 PO 4 .…”

Section: Methodsmentioning

confidence: 99%

Potential Cardioprotective Role of Menaquinone-4 Against Cardiac Ischemia–reperfusion Injury

Hadhoud

Elmahdi

Elkattawy

2023

Journal of Cardiovascular Pharmacology

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:Myocardial infarction is among the leading causes of mortality. Menaquinone-4 (MK-4), a vitamin K2 analog, might play a role in rescuing cardiac ischemia/reperfusion (I/R) injury. This work aimed to discover the potential cardioprotective role of MK-4 against myocardial I/R injury in rats. Thirty-two rats were categorized into 3 groups: (I/R) control group: subjected to I/R protocol (received vehicle), MK-4 preconditioning group: MK-4 infusion for 20 minutes before the I/R protocol, and MK-4 postconditioning group: MK-4 infusion for 20 minutes at the start of the reperfusion phase. The hearts were placed in the Langendorff apparatus, and the left ventricular developed pressure (LVDP), heart rate (HR), + (LV dP/dt) max, − (LV dP/dt) max, and Tau were calculated. The necrotic mass was determined by staining it with nitro blue tetrazolium. Creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C- reactive protein (CRP), as well as cardiac superoxide dismutase (SOD), nitric oxide (NOx), malondialdehyde (MDA), and glutathione (GSH) levels were all evaluated. MK-4 postconditioning significantly reduced myocardial infarct size; increased LVDP, + (LV dp/dt) max, − (LV dp/dt) max, and HR; reduced Tau, CK-MB, LDH, CRP, IL-6, TNF-α, MDA, and NOx levels; and increased SOD activity, whereas no significant difference in the GSH level was detected. In conclusion, these data imply that MK-4 may protect the heart from the consequences of I/R.

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“…Hepcidin is an antimicrobial protein that controls iron metabolism in mammals [ 141 ]. Hepcidin also decreases oxidative stress in rats with myocardial infarction [ 81 ]. The RA expresses greater gene expression of hepcidin than the LA [ 20 ].…”

Section: Mechanisms Contributing To the Regional Diversities Of Atrial Fibrogenesismentioning

confidence: 99%

Regional Diversities in Fibrogenesis Weighed as a Key Determinant for Atrial Arrhythmogenesis

et al. 2021

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Atrial fibrosis plays a key role in atrial myopathy, resulting in the genesis of atrial fibrillation (AF). The abnormal distribution of fibrotic tissue, electrical coupling, paracrine interactions, and biomechanical–electrical interactions have all been suggested as causes of fibrosis-related arrhythmogenesis. Moreover, the regional difference in fibrogenesis, specifically the left atrium (LA) exhibiting a higher arrhythmogenesis and level of fibrosis than the right atrium (RA) in AF, is a key contributor to atrial arrhythmogenesis. LA fibroblasts have greater profibrotic cellular activities than RA fibroblasts, but knowledge about the regional diversity of atrial regional fibrogenesis remains limited. This article provides a comprehensive review of research findings on the association between fibrogenesis and arrhythmogenesis from laboratory to clinical evidence and updates the current understanding of the potential mechanism underlying the difference in fibrogenesis between the LA and RA.

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The Effect of Hepcidin on Cardiac Ischemia-Reperfusion Injury

Cited by 5 publications

References 36 publications

Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity via modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways

Phosphodiesterase inhibitor, Vinpocetine, guards against doxorubicin induced cardiotoxicity via modulation of HIF/VEGF and cGMP/cAMP/SIRT signaling pathways

Potential Cardioprotective Role of Menaquinone-4 Against Cardiac Ischemia–reperfusion Injury

Regional Diversities in Fibrogenesis Weighed as a Key Determinant for Atrial Arrhythmogenesis

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