Mollification of Doxorubicin (DOX)-Mediated Cardiotoxicity Using Conjugated Chitosan Nanoparticles with Supplementation of Propionic Acid

Abstract

Doxorubicin is an extensively prescribed antineoplastic agent. It is also known for adverse effects, among which cardiotoxicity tops the list. The possible mechanism underlying doxorubicin (DOX)-mediated cardiotoxicity has been investigated in this study. Further, to reduce the DOX-mediated cardiotoxicity, DOX was conjugated with Chitosan Nanoparticles (DCNPs) and supplemented with propionic acid. Initially, the drug loading efficacy and conjugation of DOX with chitosan was confirmed by UV–Visible Spectroscopy (UV) and Fourier Transform Infrared Spectroscopy (FTIR). The average sizes of the synthesized Chitosan Nanoparticles (CNPs) and DCNPs were measured by Dynamic Light Scattering (DLS) analysis as 187.9 ± 1.05 nm and 277.3 ± 8.15 nm, respectively, and the zeta potential values were recorded as 55.2 ± 0.7 mV and 51.9 ± 1.0 mV, respectively. The size and shape of CNPs and DCNPs were recorded using a High-Resolution Electron Microscopy (HRTEM). The particles measured <30 nm and 33–84 nm, respectively. The toxic effects of DCNPs and propionic acid were evaluated in rat model. The data from the electrocardiogram (ECG), cardiac biomarkers, Peroxisome proliferator-activated receptor gamma (PPARγ) and histological observations indicated evidence of DOX-mediated cardiotoxicity, whereas the administration of DCNPs, as well as Propionic Acid (PA), brought about a restoration to normalcy and offered protection in the context of DOX-induced cardiotoxicity.

Jingzhi Guanxin Oral Liquids Attenuate Atherosclerotic Coronary Heart Disease via Modulating Lipid Metabolism and PPAR-Related Targets

“…Inhibition of PPARα enhances FASN levels, which mediates the first step in fatty acid synthesis [ 54 ]. PPARγ primarily facilitates the cellular uptake of lipids via anabolic pathways, and its activation gives rise to the upregulation of genes that mediate fatty acid uptake and trapping [ 55 , 56 , 57 , 58 ]. However, treatment with high-affinity agonist ligands for PPARγ, such as thiazolidinedione antidiabetic drugs, proved vasoprotective and reduced atherosclerosis in mouse models [ 59 ].…”

Box–Behnken Design: Optimization of Proanthocyanidin-Loaded Transferosomes as an Effective Therapeutic Approach for Osteoarthritis

“…A UV–visible spectrophotometer (UV 1800 Shimadzu, Kyoto, Japan) was used to detect absorbance at 278 nm after centrifugation, and 1 mL of the supernatant was diluted by the addition of 9 mL of phosphate saline buffer (pH 7.4) [ 26 ]. The efficiency of drug entrapment was determined [ 27 ] as follows: where PEE is the drug entrapment efficiency, W T is the total quantity of drug in the transferosomal suspensions, and W F is the free drug in the supernatants.…”

ULK1 Mediated Autophagy-Promoting Effects of Rutin-Loaded Chitosan Nanoparticles Contribute to the Activation of NF-κB Signaling Besides Inhibiting EMT in Hep3B Hepatoma Cells

“…The rCNPs were synthesized following methods published previously with slight modifications. [67][68][69] Chitosan was prepared at the concentration of 2 mg/mL in 2% glacial acetic acid and 50 mM sodium chloride and stirred using a magnetic stirrer for 1 hr at 300 rpm. The formed solution was visibly clear and free of residues and therefore no other processes such as filtration were adopted.…”