Melatonin improves nitric oxide bioavailability in isoproterenol induced myocardial injury

Mol Cell Endocrinol. 2024 Sep 15:591:112279. doi: 10.1016/j.mce.2024.112279. Epub 2024 May 24.

Abstract

Isoproterenol administration is associated with cardiac inflammation and decreased NO availability. Melatonin has been reported to have cardioprotective effect. The aim of this study was to investigate the effect of melatonin on NO bioavailability and inflammation in myocardial injury induced by isoproterenol. Isoproterenol was administrated in male Wistar rats for 7 days to induce cardiac injury. The animals were divided into 3 groups: Control, Isoproterenol, Isoproterenol + Melatonin. Animals received melatonin for 7 days. Echocardiographic analysis was performed and the hearts were collected for molecular analysis. Animals that received isoproterenol demonstrated a reduction in left ventricle systolic and diastolic diameter, indicating the presence of concentric hypertrophy. Melatonin was able to attenuate this alteration. Melatonin also improved NO bioavailability and decreased NF-κβ, TNFα and IL-1β expression. In conclusion, melatonin exhibited a cardioprotective effect which was associated with improving NO bioavailability and decreasing the pro-inflammatory proteins.

Keywords: Isoproterenol; Melatonin; Nitric oxide.

MeSH terms

  • Animals
  • Biological Availability*
  • Cardiotonic Agents / pharmacology
  • Heart Injuries / chemically induced
  • Heart Injuries / metabolism
  • Heart Injuries / pathology
  • Interleukin-1beta / metabolism
  • Isoproterenol*
  • Male
  • Melatonin* / pharmacology
  • Myocardium / metabolism
  • Myocardium / pathology
  • NF-kappa B / metabolism
  • Nitric Oxide* / metabolism
  • Rats
  • Rats, Wistar*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Isoproterenol
  • Melatonin
  • Nitric Oxide
  • Cardiotonic Agents
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Interleukin-1beta