ABC | Volume 114, Nº1, January 2019

Original Article Alegre et al. Açaí and myocardial ischemia-reperfusion in rats Arq Bras Cardiol. 2020; 114(1):78-86 Figure 2 – Protein expression evaluated by Western blot. C: control group; A: açaí group; SIRT1: silent information regulator 1; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; FOXO1: forkhead protein 1; aFOXO1: acetylated forkhead protein 1; Nrf-2: nuclear factor erythroid 2; NF-kB: nuclear factor kappa B; pNF-kB: phosphorylated nuclear factor kappa B. All proteins expressions were normalized by GAPDH. There are no differences between groups in protein expression (p > 0.05). 100 80 60 40 20 0 100 80 60 40 20 0 100 80 60 40 20 0 100 80 60 40 20 0 100 120 80 60 40 20 0 100 120 80 60 40 20 0 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 0.0 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 0.0 SIRT1 GAPDH Nrf2 GAPDH NF-kB GAPDH pNF-kB GAPDH FOXO1 GAPDH aFOXO1 GAPDH C A C A C A C A C A C A C A C A SIRT1/GAPDH FOXO1/GAPDH FOXO1/aFOXO1 aFOXO1/GAPDH Nrf2/GAPDH NF-kB/GAPDH pNF-kB/GAPDH NF-kB/pNF-kB Table 3 – Myocardial activity of enzymes related to energy metabolism after global ischemia-reperfusion protocol C (n= 9) A (n=10) p-value β-hydroxyacyl-CoA dehydrogenase (nmoL/mg protein) 19.8 ± 3.3 49.8 ± 7.0 < 0.001 Phosphofructokinase (nmoL/g tissue) 181 (160 – 228) 73 (67 – 82) < 0.001 Lactate dehydrogenase (nmoL/mg protein) 147 (145 – 167) 70 (65 - 77) < 0.001 Pyruvate dehydrogenase (nmoL/g tissue) 114 ± 11 176 ± 19 < 0.001 Citrate synthase (nmol/mg protein) 30 (30 – 37) 100 (81 – 117) < 0.001 Complex I (nmol/mg protein) 3.7 ± 1.0 8.0 ± 1.7 < 0.001 Complex II (nmol/mg protein) 2.1 ± 0.6 3.5 ± 0.5 < 0.001 ATP synthase (nmol/mg protein) 22.0 ± 3.9 44.5 ± 6.6 < 0.001 C: control group; A: açaí group. Values are expressed as the means ± standard deviation or median and 1st and 3rd quartile; p-value: t test or Mann-Whitney test. sources, and the energetic metabolism, more precisely the mitochondrial electron transport chain (ETC), is one of the most important generators of these radicals. 5 The continuous production of ERs during metabolic processes is regulated by an antioxidant defense system, which limits the intracellular levels and controls the occurrence of cellular damage. The antioxidant defense system can be enzymatic and non-enzymatic. 6,7,28 Non-enzymatic defense system includes antioxidant compounds of dietary origin, like vitamins, mineral and phenolic compounds. Flavonoids and other compounds present in açaí can act as non-enzymatic antioxidant, inactivating reactive species. 29 During ischemia, there is an increase in nicotinamide adenine dinucleotide oxidase, nitric oxide synthase, xanthine oxidase, cytochrome P450 and cyclooxygenase, 8,30 which may result in increased ER generation; likewise, ischemia is associated with a decrease in different antioxidant enzymes. All these changes may result in oxidative stress. In this study, 82