Curcumin conjugated zinc nanoparticles for the treatment of myocardial infarction

A modern cardioprotective drug was created by utilizing zinc nanoparticles (ZnNPs) containing curcumin to address isoproterenol-induced myocardial infarction in mice, with a specific focus on the PPAR-γ/NF-κB pathway. During the in vivo study, mice were subjected to myocardial infarction by subcutaneously administering isoproterenol at a dosage of 40 mg/kg every 12 h for a total of three administrations. The mice were randomly divided into five groups: (I, II) isoproterenol + ZnNPs at different concentrations (10, 40 μg/mL) and time intervals, (III) isoproterenol alone, and (IV) control group. Various physicochemical methods, including FT-IR, field emission scanning electron microscopy, X-Ray diffraction analysis, fourier-transform infrared spectroscopy and energy dispersive X-ray spectroscopy, were utilized to analyze and characterize the ZnNPs. The real-time PCR and western blot methods were used to examine the PPAR-γ/NF-κB activation by lipopolysaccharide (LPS) and the subsequent cytokine release. This research focused on investigating the inflammatory responses and cell apoptosis in human coronary artery endothelial cells treated with LPS. After the therapy, cardiac function was checked using an electrocardiogram, along with biochemical and histochemical analysis. The introduction of ZnNPs leads to a decrease in the inflammatory conditions present in the hearts of mice suffering from myocardial infarction. The use of ZnNPs not only enhances ventricular wall infarction but also reduces mortality rates and suppresses levels of myocardial injury markers. The usual ST segment depression observed in mice with myocardial infarction is markedly reduced when treated with ZnNPs. The mice with myocardial infarction in the pre + post-isoproterenol group seemed to experience more pronounced cardioprotective effects from the treatment with ZnNPs compared to those in the post-isoproterenol group. In an in vitro experiment, the use of ZnNPs resulted in a significant reduction in cell death and inhibition of inflammation cytokine expression. The gene expression normalization for PPAR-γ/NF-κB/IκB-α/IKKα/β and the phosphorylation of PPAR-γ could potentially be associated with the beneficial effects of ZnNPs. The rise in inflammatory responses was effectively prevented. The results of this study indicate that ZnNPs have cardioprotective efficacies on isoproterenol-induced myocardial infarction. This positive impact could be linked to the PPAR-γ activation and the NF-κB signaling inhibition.