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

  • Dose Response. 2024 Apr 18;22(2):15593258241247980. doi: 10.1177/15593258241247980.
Ahlam M Alhusaini  1 Hanan K Alghibiwi  1 Wedad S Sarawi  1 Juman S Alsaab  1 Samiyah M Alshehri  1 Qamraa H Alqahtani  1 Aliah R Alshanwani  2 Ebtesam A Aljassas  3 Ebtesam N Alsultan  3 Iman H Hasan  1
Affiliations
  • 1. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
  • 2. Department of Physiology, College of Medicine and King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia.
  • 3. Department of Pharmacognosy, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Abstract

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.

Keywords
L-resveratrol; S100 A; apoptosis; isoproterenol; myocardial infarction.