d-Limonene Ameliorates Myocardial Infarction Injury by Reducing Reactive Oxygen Species and Cell Apoptosis in a Murine Model

J Nat Prod. 2019 Nov 22;82(11):3010-3019. doi: 10.1021/acs.jnatprod.9b00523. Epub 2019 Nov 11.

Abstract

Myocardial infarction (MI) leads to high mortality, and pharmacological or percutaneous primary interventions do not significantly inhibit ischemia/reperfusion injuries, particularly those caused by oxidative stress. Recently, research groups have evaluated several naturally occurring antioxidant compounds for possible use as therapeutic alternatives to traditional treatments. Studies have demonstrated that d-limonene (DL), a monoterpene of citrus fruits, possesses antioxidant and cardiovascular properties. Thus, this work sought to elucidate the mechanisms of protection of DL in an isoproterenol-induced murine MI model. It was observed that DL (10 μmol) attenuated 40% of the ST elevation, reduced the infarct area, prevented histological alterations, abolished completely oxidative stress damage, restored superoxide dismutase activity, and suppressed pro-apoptotic enzymes. In conclusion, the present study demonstrated that DL produces cardioprotective effects from isoproterenol-induced myocardial infarction in Swiss mice through suppression of apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / therapeutic use*
  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / drug effects
  • Apoptosis Regulatory Proteins / metabolism
  • Electrocardiography / drug effects
  • Limonene / therapeutic use*
  • Long QT Syndrome / prevention & control
  • Male
  • Mice
  • Molecular Structure
  • Myocardial Infarction / drug therapy*
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism*
  • Superoxide Dismutase / metabolism

Substances

  • Antioxidants
  • Apoptosis Regulatory Proteins
  • Reactive Oxygen Species
  • Limonene
  • Superoxide Dismutase