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. 2021 Jul 29:2021:3394348.
doi: 10.1155/2021/3394348. eCollection 2021.

Chitosan and Curcumin Nanoformulations against Potential Cardiac Risks Associated with Hydroxyapatite Nanoparticles in Wistar Male Rats

Israa F Mosa  1 , Haitham H Abd  2 , Abdelsalam Abuzreda  3 , Amenh B Yousif  4 , Nadhom Assaf  5
Affiliations

Chitosan and Curcumin Nanoformulations against Potential Cardiac Risks Associated with Hydroxyapatite Nanoparticles in Wistar Male Rats

Israa F Mosa et al. Int J Biomater. .

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.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
TEM micrographs of needle like nano-HAP.
Figure 2
Figure 2
TEM micrographs and size distribution of CsNPs.
Figure 3
Figure 3
TEM micrographs and size distribution of CurNPs.
Figure 4
Figure 4
Mean values ± SE of heart levels of vascular endothelial growth factor-A (VEGF-A), cyclooxygenase-2 (COX-2 expression), and atrial natriuretic factor (ANF expression).
Figure 5
Figure 5
Mean values ± SE of heart thiobarbituric acid-reactive substances and nitric oxide.
Figure 6
Figure 6
Mean values ± SE of heart glutathione peroxidase, glutathione S-transferase, catalase, superoxide dismutase, total antioxidant capacity, and reduced glutathione.
Figure 7
Figure 7
Mean values ± SE of heart creatine kinase-muscle/brain and lactate dehydrogenase.
Figure 8
Figure 8
Mean values ± SE of cholesterol, triglyceride, high-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and low-density lipoprotein cholesterol.
Figure 9
Figure 9
Mean values ± SE of heart levels of tumor suppressor P53, tumor necrosis factor-α, and interleukin-6.
Figure 10
Figure 10
(a–h) Photomicrographs of rat left ventricle section in different experimental groups stained with Haematoxylin and Eosin.
Figure 11
Figure 11
(a–h) Photomicrographs of rat myocardium section in different experimental groups stained with PCNA-ir.
See this image and copyright information in PMC

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