Abstract

The cardiac remodeling after myocardial infarction is characterized by inflammation and oxidative stress. Thus, this study aimed to test the hypothesis that jaboticaba, due to its anti-inflammatory and antioxidants properties, attenuates cardiac remodeling after myocardial infarction. Wistar rats were submitted to myocardial infarction due to coronary artery occlusion, and divided into four experimental groups: C, sham control animals; I, animals submitted to myocardial infarction, received a standard diet; IJ2, animals submitted to myocardial infarction, received a standard diet plus 2% jaboticaba; and IJ4, animals submitted to myocardial infarction, received a standard diet plus 4% jaboticaba. After a three-month follow-up, echocardiography, histology, oxidative stress, and cardiac energy metabolism were analyzed. There was no difference in infarct size or mortality among the infarcted groups. The IJ4 group displayed improved diastolic function, as assessed by isovolumetric relaxation time normalized to the heart rate. As expected, the percentage of collagen was higher in all infarcted groups than in the C group. However, the IJ2 group had less collagen than groups I and IJ4. The IJ4 group presented lower PFK activity than I and IJ2, and lower pyruvate dehydrogenase activity than controls, whereas the IJ2 group showed no differences compared to the control group in both LDH and ATP synthase activity. The 2% and 4% doses attenuated lipid peroxidation and increased the activity of glutathione peroxidase compared with the I group. In conclusion, jaboticaba attenuated the remodeling process after myocardial infarction, which was associated with decreased oxidative stress and improved energy metabolism.

Highlights

  • Introduction published maps and institutional affilAfter myocardial infarction (MI), complex changes in ventricular architecture can occur, including cavity dilation, hypertrophy, and fibrosis of non-infarcted regions

  • Our results showed that jaboticaba attenuated the remodeling process after myocardial infarction, which was associated with decreased oxidative stress and improved energy metabolism

  • The animals were allocated into four experimental groups and observed for three months: C (n = 16), sham control animals; I (n = 37), animals submitted to myocardial infarction, received standard diet; IJ2 (n = 36), animals submitted to myocardial infarction, received standard diet plus 2% jaboticaba; and IJ4 (n = 37), animals submitted to myocardial infarction, received standard diet plus 4% jaboticaba

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Summary

Introduction

After myocardial infarction (MI), complex changes in ventricular architecture can occur, including cavity dilation, hypertrophy, and fibrosis of non-infarcted regions. This overall process of alterations in ventricular size, composition, and mass is known as ventricular remodeling [1,2,3]. Several strategies are already consolidated in the prevention of remodeling, this process continues to occur in a large number of patients after coronary occlusion [4]. Several mechanisms modulate cardiac remodeling after MI, including neurohormonal activation, increase in cell death by apoptosis and autophagy, alterations in the contractile proteins, alterations in the calcium transport system, collagen accumulation, changes in matricellular proteins, metalloproteases activation, inflammation, oxidative stress, and iations

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