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.

中文翻译：

---

Spondias mombin L.可减轻与氧化应激和炎症调节相关的心肌梗塞后的心室重构。

这项研究的目的是评估Spondias mombinL.（SM）牙髓及其对心肌梗死（MI）后心脏重构的影响。将Wistar雄性大鼠分为四组：假组（动物接受模拟手术），接受标准食物（S； n = 20）；梗死组，接受标准食物（MI； n = 24），梗死组补充维生素C 100 mg SM / kg体重/ d（MIS100; n = 23）和梗死组补充250 mg SM / kg体重/ d（MIS250; n = 22）。治疗3个月后，进行了形态，功能和生化分析。MI引起左心室结构和功能改变与不断恶化的收缩和舒张功能，并以不同的剂量并没有影响这些变量SM补充超声心动图和离体心脏研究（如分析P > .05）。但是，补充SM可以减轻MI后的心脏重塑，减少纤维化（P  = .047）和肥大（P  = .006）。在心肌组织中进一步研究了氧化应激，炎症过程和能量代谢的生物标志物。SM补充改善了心肌的能量代谢效率，并降低了脂质过氧化氢[S组（n = 8）：267.26±20.7；MI组（n = 8）：330.14±47.3; MIS100组（n = 8）：313.8±46.2; MIS250组：294.3±38.0 nmol / mg组织; P = .032]，以及MI后炎症通路的激活减少。总之，SM补充可减轻MI后的心脏重塑过程。我们还发现能量代谢，氧化应激和炎症与这种作用有关。此外，以最高剂量补充SM更有效。