Abstract

BackgroundMyocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. Dietary intervention on adverse cardiac remodeling after MI has significant clinical relevance. Rosemary leaves are a natural product with antioxidant/anti-inflammatory properties, but its effect on morphology and ventricular function after MI is unknown.Methods and resultsTo determine the effect of the dietary supplementation of rosemary leaves on cardiac remodeling after MI, male Wistar rats were divided into 6 groups after sham procedure or experimental induced MI: 1) Sham group fed standard chow (SR0, n = 23); 2) Sham group fed standard chow supplemented with 0.02% rosemary (R002) (SR002, n = 23); 3) Sham group fed standard chow supplemented with 0.2% rosemary (R02) (SR02, n = 22); 4) group submitted to MI and fed standard chow (IR0, n = 13); 5) group submitted to MI and fed standard chow supplemented with R002 (IR002, n = 8); and 6) group submitted to MI and fed standard chow supplemented with R02 (IR02, n = 9). After 3 months of the treatment, systolic pressure evaluation, echocardiography and euthanasia were performed. Left ventricular samples were evaluated for: fibrosis, cytokine levels, apoptosis, energy metabolism enzymes, and oxidative stress. Rosemary dietary supplementation attenuated cardiac remodeling by improving energy metabolism and decreasing oxidative stress. Rosemary supplementation of 0.02% improved diastolic function and reduced hypertrophy after MI. Regarding rosemary dose, 0.02% and 0.2% for rats are equivalent to 11 mg and 110 mg for humans, respectively.ConclusionOur findings support further investigations of the rosemary use as adjuvant therapy in adverse cardiac remodeling.

Highlights

  • Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide

  • To determine the effect of the dietary supplementation of rosemary leaves on cardiac remodeling after MI, male Wistar rats were divided into 6 groups after sham procedure or experimental induced MI: 1) Sham group fed standard chow (SR0, n = 23); 2) Sham group fed standard chow supplemented with 0.02% rosemary (R002) (SR002, n = 23); 3) Sham group fed standard chow supplemented with 0.2% rosemary (R02) (SR02, n = 22); 4) group submitted to MI and fed standard chow (IR0, n = 13); 5) group submitted to MI and fed standard chow supplemented with R002 (IR002, n = 8); and 6) group submitted to MI and fed standard chow supplemented with R02 (IR02, n = 9)

  • The death of myocytes initiates a cascade of intracellular signaling, such as inflammation, oxidative stress, reabsorption of necrotic tissue, excessive deposition of collagen, and hypertrophy, that can result in adverse cardiac remodeling

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Summary

Introduction

Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. The death of myocytes initiates a cascade of intracellular signaling, such as inflammation, oxidative stress, reabsorption of necrotic tissue, excessive deposition of collagen, and hypertrophy, that can result in adverse cardiac remodeling. These molecular, cellular and interstitial changes can clinically be manifested as changes in size, mass, geometry and heart function. Cardiac remodeling is an adaptation of the heart to aggression stimuli that may gradually lead to the development of heart failure (HF), responsible for the increased mortality after MI[2, 3]. Rosemary leaves are a natural product with antioxidant/anti-inflammatory properties, but its effect on morphology and ventricular function after MI is unknown

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