Protective effect of nicorandil against myocardial ischemia/reperfusion injury mediated via IL33/ST2 signaling pathway

Zheng, Yi; Li, Xueyin; Zhang, Fan; Zhao, Bo; Du, Wanting; Sun, De‐Zheng; Li, Guangping

doi:10.1007/s11010-022-04418-z

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…The myocardium contributes to the role of the heart in promoting blood circulation, which is vital to human health. Myocardial damage can cause myocardial dysfunction, leading to cardiac failure and even death . Meanwhile, the myocardium is a protein-abundant muscle tissue with a rich amino acid composition, which can be a high-quality raw material for preparing biologically activated peptides.…”

Section: Discussionmentioning

confidence: 99%

“…Myocardial injury may contribute to cardiovascular diseases and result in myocardial structural changes and myocardial dysfunction . Myocardial dysfunction is considered to be a major causative factor of myocarditis, myocardial infarction, and other diseases. , Myocardial injury is the main pathological cause of heart failure, which is the main cause of death from cardiovascular disease . While most drugs used to reduce myocardial damage are dextroproimide and dexmedetomidine, which would cause side effects, such as low blood pressure and nausea, it is of great significance to develop safe active substances with cardioprotective function.…”

Section: Introductionmentioning

confidence: 99%

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Peptide Characterization of Bovine Myocardium Hydrolysates and Its Ameliorative Effects on Doxorubicin-Induced Myocardial Injury in H9c2 Cells and in Mice

Li,

Lv,

Zhang

et al. 2023

J. Agric. Food Chem.

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The prevalence and mortality of heart disease have a persistent existence, and it is important to develop active substances with cardioprotective properties. It has been reported that peptides from animal heart hydrolysates possess cardioprotective activity, but those mechanisms and the sequence of peptides are still unrevealed. In the present study, the extracts of bovine myocardium were prepared by enzymatic hydrolysis (BHH-A) and water extraction (BHH-W). The cardioprotective function of peptides was verified in the DOX-induced H9c2 cells and myocardial injury mice. The mass spectrometry was used to contrast the differences of active ingredients between BHH-W and BHH-A. Results suggested that both BHH-A and BHH-W could increase the activity of antioxidant enzymes in cardiomyocytes and reduce the inflammatory level and apoptosis of myocardial cells. The improvement effects of BHH-A on myocardial injury in mice were better than those of BHH-W. The analysis of peptide composition demonstrated that the contents with N-segment hydrophobic amino acids were higher in the peptides identified in BHH-A. Hence, BHH-A could be used as a potential active substance to improve DOX-induced myocardial injury by reducing oxidative damage, inflammation, and cardiomyocyte apoptosis, and its activity may be related to the richness of small molecular peptides and hydrophobic amino acids.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Peptide Characterization of Bovine Myocardium Hydrolysates and Its Ameliorative Effects on Doxorubicin-Induced Myocardial Injury in H9c2 Cells and in Mice

Li,

Lv,

Zhang

et al. 2023

J. Agric. Food Chem.

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“…The results of this study are based on in vitro experiments with a commercial rat heart-derived cell line (H9c2) that is characterized by a permanent division ability but still retains some cardiomyocyte characteristics. Although the use of H9c2 cells has been recognized as a valid and suitable in vitro model for simulating various cardiac pathological processes, including ischemia and reperfusion injury [ 53 , 54 , 55 ], they cannot perfectly recapitulate the characteristics of primary cardiomyocyte cultures. Moreover, the involvement of sialidase-3 in the cardiac response to IRI in vivo has been studied only in terms of mRNA expression.…”

Section: Study Limitationsmentioning

confidence: 99%

Neu3 Sialidase Activates the RISK Cardioprotective Signaling Pathway during Ischemia and Reperfusion Injury (IRI)

Piccoli

Coviello

Canali

et al. 2022

IJMS

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Coronary reperfusion strategies are life-saving approaches to restore blood flow to cardiac tissue after acute myocardial infarction (AMI). However, the sudden restoration of normal blood flow leads to ischemia and reperfusion injury (IRI), which results in cardiomyoblast death, irreversible tissue degeneration, and heart failure. The molecular mechanism of IRI is not fully understood, and there are no effective cardioprotective strategies to prevent it. In this study, we show that activation of sialidase-3, a glycohydrolytic enzyme that cleaves sialic acid residues from glycoconjugates, is cardioprotective by triggering RISK pro-survival signaling pathways. We found that overexpression of Neu3 significantly increased cardiomyoblast resistance to IRI through activation of HIF-1α and Akt/Erk signaling pathways. This raises the possibility of using Sialidase-3 activation as a cardioprotective reperfusion strategy after myocardial infarction.

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Mechanisms of the “No-Reflow” Phenomenon After Acute Myocardial Infarction

Kaul

Methner²,

Cao³

et al. 2023

JACC: Basic to Translational Science

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Protective effect of nicorandil against myocardial ischemia/reperfusion injury mediated via IL33/ST2 signaling pathway

Cited by 4 publications

References 22 publications

Peptide Characterization of Bovine Myocardium Hydrolysates and Its Ameliorative Effects on Doxorubicin-Induced Myocardial Injury in H9c2 Cells and in Mice

Peptide Characterization of Bovine Myocardium Hydrolysates and Its Ameliorative Effects on Doxorubicin-Induced Myocardial Injury in H9c2 Cells and in Mice

Neu3 Sialidase Activates the RISK Cardioprotective Signaling Pathway during Ischemia and Reperfusion Injury (IRI)

Mechanisms of the “No-Reflow” Phenomenon After Acute Myocardial Infarction

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