<p>Myocardial infarction (MI) is recognized by its rapid onset and higher mortality rate. The intricate nature of its pathological process has rendered targeted therapy for MI a persistent issue. Hesperidin (HES) has been identified that may protect cardiac cells and promote myocardial tissue regeneration. Nonetheless, its effectiveness in addressing MI-related ischemia situations is hindered by its insufficient angiogenesis and poor bioavailability. This present investigation demonstrates that the effective therapy of HES is augmented by mesoporous copper carbonate (MCC) microspheres, owing to their superior drug-delivery capacity and consistent release of angiogenic degradation (Cu). The cellular examinations demonstrated that HES and Cu could produce synergic effects on endothelial cell angiogenesis and anti-cardiomyocyte apoptosis. Additionally, an in vivo MI model showed that the HES-loaded MCC (MCC@HES) significantly reduced cardiomyocyte apoptosis, decreased infarct size, and enhanced vascularization in myocardial tissue. Overall, the present study is groundbreaking for indicating the benefits of integrating HES with MCC nanocarriers for myocardial remodeling and for presenting an innovative, meticulously designed MCC@HES system as a prospective treatment approach for MI.</p>

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Cardioprotective effects of hesperidin-loaded biodegradable mesoporous copper to reduce cardiomyocyte apoptosis for myocardial infarction

  • Man Liu,
  • Songze Wu

摘要

Myocardial infarction (MI) is recognized by its rapid onset and higher mortality rate. The intricate nature of its pathological process has rendered targeted therapy for MI a persistent issue. Hesperidin (HES) has been identified that may protect cardiac cells and promote myocardial tissue regeneration. Nonetheless, its effectiveness in addressing MI-related ischemia situations is hindered by its insufficient angiogenesis and poor bioavailability. This present investigation demonstrates that the effective therapy of HES is augmented by mesoporous copper carbonate (MCC) microspheres, owing to their superior drug-delivery capacity and consistent release of angiogenic degradation (Cu). The cellular examinations demonstrated that HES and Cu could produce synergic effects on endothelial cell angiogenesis and anti-cardiomyocyte apoptosis. Additionally, an in vivo MI model showed that the HES-loaded MCC (MCC@HES) significantly reduced cardiomyocyte apoptosis, decreased infarct size, and enhanced vascularization in myocardial tissue. Overall, the present study is groundbreaking for indicating the benefits of integrating HES with MCC nanocarriers for myocardial remodeling and for presenting an innovative, meticulously designed MCC@HES system as a prospective treatment approach for MI.