Resveratrol-Based Liposomes Improve Cardiac Remodeling Induced by Isoproterenol Partially by Modulating MEF2, Cytochrome C and S100A1 Expression

• Published in: Dose-response Vol. 22; no. 2; p. 15593258241247980
• Main Authors: Alhusaini, Ahlam M., Alghibiwi, Hanan K., Sarawi, Wedad S., Alsaab, Juman S., Alshehri, Samiyah M., Alqahtani, Qamraa H., Alshanwani, Aliah R., Aljassas, Ebtesam A., Alsultan, Ebtesam N., Hasan, Iman H.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01-04-2024; SAGE PUBLICATIONS, INC; SAGE Publishing
• Subjects: Cytochrome; Disease prevention; Gene expression; Heart failure; Inflammation; Intervention; Laboratory animals; Oxidative stress; apoptosis; isoproterenol; S100 A; L-resveratrol; myocardial infarction
• ISSN: 1559-3258; 1559-3258
• DOI: 10.1177/15593258241247980

Isoproterenol (ISO), a chemically synthesized catecholamine, belongs to β-adrenoceptor agonist used to treat bradycardia. The β-adrenergic agonist is an essential regulator of myocardial metabolism and contractility; however, excessive exposure to ISO can initiate oxidative stress and inflammation. This study aims to investigate the molecular mechanisms underlying ISO-induced cardiac remodeling, the protective efficacy of resveratrol (RSVR), and its liposomal formulation (L-RSVR) against such cardiac change. Wistar albino rats were evenly divided into 4 groups. Control group, ISO group received ISO (50 mg/kg, s.c.) twice a week for 2 weeks, and RSVR- and L-RSVR-treated groups in which rats received either RSVR or L-RSVR (20 mg/kg/day, p.o.) along with ISO for 2 weeks. ISO caused a significant elevation of the expression levels of BAX and MEF2 mRNA, S100A1 and cytochrome C proteins, as well as DNA fragmentation in cardiac tissue compared to the control group. Treatment with either RSVR or L-RSVR for 14 days significantly ameliorated the damage induced by ISO, as evidenced by the improvement of all measured parameters. The present study shows that L-RSVR provides better cardio-protection against ISO-induced cardiac injury in rats, most likely through modulation of cardiac S100A1 protein expression and inhibition of inflammation and apoptosis.