Short term inhalation of cigarette smoke (CS) induces significant lung inflammation due to an imbalance of oxidant/antioxidant mechanisms. Açai fruit (Euterpe oleracea) has significant antioxidant and anti-inflammatory actions. The present study aimed to determine whether oral administration of an açai stone extract (ASE) could reduce lung inflammation induced by CS. Thirty C57BL/6 mice were assigned to three groups (n=10 each): the Control+A group was exposed to ambient air and treated orally with ASE 300 mg/kg/day; the CS group was exposed to smoke from 6 cigarettes per day for 5 days; and the CS+A group was exposed to smoke from 6 cigarettes per day for 5 days and treated orally with ASE (300 mg/kg/day). On day 6, all mice were sacrificed. After bronchoalveolar lavage, the lungs were removed for histological and biochemical analyses. The CS group exhibited increases in alveolar macrophage (AMs) and neutrophil numbers (PMNs), myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities (GPx), TNF-α expression, and nitrites levels in lung tissue when compared with the control ones (p<0.001 for all parameters). The AMs, PMNs, MPO, SOD, CAT, GPx and nitrite were significantly reduced by oral administration of ASE when compared with CS group (p<0.001 for all parameters, with exception of AMs p<0.01). The present results suggested that systemic administration of an ASE extract could reduce the inflammatory and oxidant actions of CS. Thus, the results of this study in mice should stimulate future studies on ASE as a potential agent to protect against CS-induced inflammation in humans.

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Dengue virus infection is a major cause of human arbovirosis, for which clinical and experimental evidence supports the idea that liver dysfunction and lipid metabolism disorders are characteristics of severe disease. Analyzing mitochondrial bioenergetics, here we show that infection of hepatic cells with dengue virus favors the cellular capacity of metabolizing glucose, impairing the normal metabolic flexibility that allows the oxidative machinery to switch among the main energetic substrates. However, instead of being used as an energy source, glucose performs an anaplerotic role in the oxidation of endogenous fatty acids, which become the main energetic substrate during infection. Taken together, the results shed light on metabolic mechanisms that may explain the profound alterations in lipid metabolism for severe dengue patients, contributing to the understanding of dengue physiopathology.

Our aim was to investigate the effects of four different statins on acute lung inflammation induced by cigarette smoke (CS). C57BL/6 male mice were divided into a control group (sham-smoked) and mice exposed to CS from 12 cigarettes/day for 5 days. Mice exposed to CS were grouped and treated with vehicle (i.p.), atorvastatin (10 mg/kg), pravastatin (10 mg/kg), rosuvastatin (5 mg/kg), or simvastatin (20 mg/kg). Treatment with statins differentially improved the pulmonary response when compared to the CS group. Atorvastatin and pravastatin demonstrated slightly effects on inflammation and oxidative stress. Rosuvastatin demonstrated the best anti-inflammatory effect, whereas simvastatin demonstrated the best antioxidant response.

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