Abstract
The objective of this study was to evaluate Spondias mombin L. (SM) pulp and its influence on cardiac remodelling after myocardial infarction (MI). Male Wistar rats were assigned to four groups: a sham group (animals underwent simulated surgery) that received standard chow (S; n = 20), an infarcted group that received standard chow (MI; n = 24), an infarcted group supplemented with 100 mg of SM/kg bodyweight/d, (MIS100; n = 23) and an infarcted group supplemented with 250 mg of SM/kg bodyweight/d (MIS250; n = 22). After 3 months of treatment, morphological, functional and biochemical analyses were performed. MI induced structural and functional changes in the left ventricle with worsening systolic and diastolic function, and SM supplementation at different doses did not influence these variables as analysed by echocardiography and an isolated heart study (P > .05). However, SM supplementation attenuated cardiac remodelling after MI, reducing fibrosis (P = .047) and hypertrophy (P = .006). Biomarkers of oxidative stress, inflammatory processes and energy metabolism were further investigated in the myocardial tissue. SM supplementation improved the efficiency of energy metabolism and decreased lipid hydroperoxide in the myocardium [group S (n = 8): 267.26 ± 20.7; group MI (n = 8): 330.14 ± 47.3; group MIS100 (n = 8): 313.8 ± 46.2; group MIS250: 294.3 ± 38.0 nmol/mg tissue; P = .032], as well as decreased the activation of the inflammatory pathway after MI. In conclusion, SM supplementation attenuated cardiac remodelling processes after MI. We also found that energy metabolism, oxidative stress and inflammation are associated with this effect. In addition, SM supplementation at the highest dose is more effective.
Highlights
Ischemic heart disease is the single most frequent cause of death worldwide.[1,2] More than 1.8 million people die each year in Europe from ischemic heart disease, mainly from myocardial infarction (MI).[1,2] MI has been defined as the focus of necrosis caused by low tissue perfusion with signs and symptoms resulting from cardiac cell death
The animals were assigned to four groups: a sham group that received standard chow (S; n = 20), an infarcted group that received standard chow (MI; n = 24), an infarcted group that received standard chow supplemented with 100 mg of Spondias mombin L. (SM)/kg bodyweight/d (MIS100; n = 23) and an infarcted group that received standard chow supplemented with 250 mg of SM/kg bodyweight/d (MIS250; n = 22)
The animals with an infarct size greater than 35% were evaluated via histology and there was no difference among the groups [MI (n = 24): 47.5 ± 1.57%; MIS100 (n = 23): 49.2 ± 1.32%; MIS250 (n = 22): 45.4 ± 1.51%; P = .268]. (Figure 1)
Summary
Ischemic heart disease is the single most frequent cause of death worldwide.[1,2] More than 1.8 million people die each year in Europe from ischemic heart disease, mainly from myocardial infarction (MI).[1,2] MI has been defined as the focus of necrosis caused by low tissue perfusion with signs and symptoms resulting from cardiac cell death It initiates a cascade of intracellular signalling that leads to molecular, cellular and interstitial changes that are manifested clinically as changes in size, shape and function of the heart. With the continuity of the process, there is a progressive ventricular dysfunction and death.[3,4,5,6]
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