ABC | Volume 114, Nº1, January 2019

Short Editorial Antioxidant Effects of Euterpe Oleracea Mart. (Açai) on Myocardial Ischemia-Reperfusion Injury in Rats: Would it Represent a Good Way To Follow? Allan Kardec Nogueira de Alencar 1 Faculdade de Medicina de Petrópolis (FMP), 1 Petrópolis, RJ – Brazil Short editorial related to the article: Euterpe Oleracea Mart. (Açaí) Reduces xidative Stress and Improves Energetic Metabolism in Myocardial Ischemia-Reperfusion Injury in Rats Mailing Address: Allan Kardec Nogueira de Alencar • Av. Barão do Rio Branco, 1003. Postal Code 25680-120, Petrópolis, RJ – Brazil E-mail: allankdc@gmail.com Keywords Euterpe Olerácea ; Oxidative Stress; Energy Metabolism; Myocardial Ischemia; Myocardial Reperfusion Injury; Rats. DOI: https://doi.org/10.36660/abc.20190770 Abrupt occlusion of an epicardial coronary artery may result in acute myocardial infarction with elevation of the ST segment as the myocardium underwent an ischemic process. 1 This promotes damage to the cardiomyocytes, mainly due to metabolic disturbances in the ATP generation with subsequent cell death andmyocardial necrosis. Furthermore, reduced levels of intracellular ATP leads to an overload of cytosolic Ca 2+ and Na + concentrations and heart function impairment. 2 It would be expected that restoration of blood flow to the ischemic area in the myocardium to minimize the injury, but reperfusion may also induce additional damage to the cardiac cells, a phenomenon described as ischemia-reperfusion (I/R) injury 3 which contributes to an increased infarct area andmicrovascular dysfunction, being sometimes lethal. 4 Myocardial I/R injury involves several features that potentiate the final damage on the heart. Morphologically, I/R lesions presents contraction bands, karyolysis, disturbance of mitochondria, sarcolemma disruption, microvascular destruction, interstitial hemorrhage, and inflammation. 5 Additionally, at reperfusion period an elevation in the production of reactive oxygen species (ROS) displays important roles for the I/R injury extent. 6 The respiratory chain and NADPH oxidases of the NOX family are major sources of ROS that trigger the opening of mitochondrial permeability pore, causing irreversible damage to the cardiomyocytes. 6 Usually, the rupture of atheroma and partial or complete obstruction of an epicardial coronary artery is followed by spontaneous or interventional reperfusion. However, reperfusion sometimes may not occur. 7 Thus, we might realize that these burdens of factors augment the final infarct size and that it is complicated to recapitulate them by using animal models considering the vast anatomic and physiological differences from the human scenario. Nevertheless, most of the current knowledge about I/R-induced myocardial damage is derived from experimental studies in animals 5 and rodent models of I/R injury can help to clarify potential pathophysiological mechanisms and identify new targets to treat this clinical condition. In this context, rat models of myocardial infarct and I/R injury have been instigating the pre-clinical research field to establish the therapeutic potential of natural agents in innumerous diseases. The antioxidant effect observed in some plant components might be useful for proposing their applicability to induce cardioprotection, and this characteristic could be, in part, proven by administrating natural products, for example, in rats with experimentally induced cardiac injury. Euterpe oleracea Mart., popularly known as “açai,” is a fruit extensively cultivated in the North region of Brazil, specifically in the Amazon. This purple fruit was chemically studied, and it was found several antioxidant substances on its composition. 8,9 Additionally, açai has anti-inflammatory and vasodilator effects. 9,10 A recent work has been performed by Alegre et al., 11 in which the authors address that açai supplementation prevents metabolism deregulation in an acute rat model of myocardial I/R injury. This study shows that preventive treatment with açai attenuates oxidative stress but did not decrease the infarcted area or improve left ventricular function after global I/R. The authors described a beneficial effect of açai only in the metabolism of heart cells and discuss that the reduction of oxidative stress would be followed by an improvement in the left ventricular function. However, they observed that the treatment with açai worsened diastolic function after I/R leading to infer that the left heart dysfunction depends on mechanisms other than oxidative damage. Additionally, despite the changes observed in antioxidant enzymes in this work, açai supplementation did not influence the expression of transcriptional factor NF- κ B, Nrf2, SIRT1, and FOXO1, proteins related with oxidative stress, regulation of the antioxidant enzymes production and cellular balance by acting on apoptosis, mitochondrial biogenesis, inflammation, glucose and lipid metabolism. I understand that this data can be justified by the protocol used in this work, as probably there was not enough time for the I/R injury to stimulate protein transcription. But, in my opinion, the preventive treatment with açai for six weeks, should have avoided, at least partially, the higher levels of some of these markers after global I/R injury in hearts from male rats, as it acts as an antioxidant agent. It is also addressed that açai supplementation led to a higher activity of β -hydroxyacyl-CoA dehydrogenase and citrate synthase enzymes which can characterize higher fatty acid oxidation. Moreover, there was a lower activity of phosphofructokinase, the enzyme for glycolysis. 11 The authors explain that açai supplementation altered substrate selection for mitochondrial oxidation in reperfusion from glucose to fatty acids, maintaining the energy metabolism closer to a physiological situation. In this regard, I perceived a contradictory discussion of the presented results as the authors 87