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Chitosan and Curcumin Nanoformulations against Potential Cardiac Risks Associated with Hydroxyapatite Nanoparticles
Israa F Mosa1, Haitham H Abd2, Abdelsalam Abuzreda3
1Department of Nanotoxicology and Animal Physiology, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt.
Abstract:
Nanoparticle-induced cardiovascular diseases have attracted much attention. Upon entering the blood circulation system, these particles have the potency to induce cardiomyocytes, leading to cardiac failure or myocardial ischemia, and the molecular mechanism remains to be completely clarified. In this study, the cardiac toxicity of rats orally exposed to hydroxyapatite nanoparticles (HAPNPs) has been observed through an increase in myocardial infarction serum markers including CK-MB and alterations in routine blood factors, expression of apoptosis-related protein P53, and increased levels of serum inflammatory markers represented by the tumor necrosis factor alpha and Interleukin-6, as well as a decline in heart antioxidant enzymes and reduced glutathione level, while an induction in lipid peroxidation and nitric oxide has been observed, as well as notable histological and histochemical alterations in the heart of these animals. mRNA and protein expressions of vascular endothelial growth factor (VEGF-A), cyclooxygenase-2 (COX-2), and atrial natriuretic factor (ANF) were elevated in the myocardium. However, the coadministration of chitosan nanoparticles (CsNPs) and/or curcumin nanoparticles (CurNPs) successfully modulated these alterations and induced activation in antioxidant parameters. The present data suggest that HAPNPs-induced apoptosis via the mitochondrial pathway may play a crucial role in cardiac tissue damage and the early treatment with CsNPs and CurNPs may protect the heart from infarction induced by HAPNPs toxic effect.
Insights
Hydroxyapatite nanoparticles (HAPNPs) cause cardiac damage by inducing apoptosis. Early treatment with chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) can protect the heart from HAPNPs toxicity.
Area of Science:
- Environmental toxicology
- Cardiovascular pathology
- Nanomedicine
Background:
- Nanoparticle exposure poses risks to cardiovascular health, potentially causing heart failure and myocardial ischemia.
- The precise molecular mechanisms underlying nanoparticle-induced cardiac toxicity are not fully understood.
Purpose of the Study:
- To investigate the cardiac toxicity of hydroxyapatite nanoparticles (HAPNPs) in rats.
- To explore the protective effects of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) against HAPNPs-induced cardiotoxicity.
Main Methods:
- Oral administration of HAPNPs to rats, followed by assessment of cardiac biomarkers, apoptosis markers, inflammatory cytokines, antioxidant enzymes, and histological changes.
- Evaluation of the effects of co-administering CsNPs and/or CurNPs.
Main Results:
- HAPNPs exposure increased myocardial infarction markers (CK-MB), P53 expression, inflammatory cytokines (TNF-α, IL-6), lipid peroxidation, and nitric oxide.
- HAPNPs decreased antioxidant enzyme activity and glutathione levels, with observed histological damage.
- Co-administration of CsNPs and/or CurNPs modulated these toxic effects and enhanced antioxidant parameters.
Conclusions:
- HAPNPs induce cardiac tissue damage and apoptosis through the mitochondrial pathway.
- Early intervention with CsNPs and CurNPs demonstrates a protective effect against HAPNPs-induced cardiotoxicity and infarction.
