Antioxidant action of propolis on mouse lungs exposed to short-term cigarette smoke.

Propolis is a natural product with antioxidant properties. In this study, we tested the efficacy of propolis against acute lung inflammation (ALI) caused by cigarette smoke (CS). C57BL6 male mice were exposed to CS and treated with propolis (200mg/kg orally, CS+P) or only with propolis (P). A Control group treated with propolis was sham-smoked (Control+P). We collected the lungs for histological and biochemical analyses. We observed an increase in alveolar macrophages and neutrophils in the CS group compared with the Control+P. These counts reduced in the CS+P group compared to the CS group. The treatment with propolis normalized all biochemical parameters in the CS+P group compared with the CS group, including nitrite, myeloperoxidase level, antioxidant enzyme activities (superoxide dismutase, catalase and glutathione peroxidase), reduced glutathione/oxidized glutathione ratio and malondialdehyde. Additionally, TNF-α expression reduced in the CS+P group when compared with the CS group. These data imply a potential antioxidant and anti-inflammatory role for propolis with regard to ALI caused by CS in mice.

Effects of Euterpe oleracea Mart. (AÇAÍ) extract in acute lung inflammation induced by cigarette smoke in the mouse.

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.

Addition of açaí (Euterpe oleracea) to cigarettes has a protective effect against emphysema in mice.

Chronic inhalation of cigarette smoke (CS) induces emphysema by the damage contributed by oxidative stress during inhalation of CS. Ingestion of açai fruits (Euterpe oleracea) in animals has both antioxidant and anti-inflammatory effects. This study compared lung damage in mice induced by chronic (60-day) inhalation of regular CS and smoke from cigarettes containing 100mg of hydroalcoholic extract of açai berry stone (CS + A). Sham smoke-exposed mice served as the control group. Mice were sacrificed on day 60, bronchoalveolar lavage was performed, and the lungs were removed for histological and biochemical analyses. Histopathological investigation showed enlargement of alveolar space in CS mice compared to CS + A and control mice. The increase in leukocytes in the CS group was higher than the increase observed in the CS + A group. Oxidative stress, as evaluated by antioxidant enzyme activities, mieloperoxidase, glutathione, and 4-hydroxynonenal, was reduced in mice exposed to CS+A versus CS. Macrophage and neutrophil elastase levels were reduced in mice exposed to CS + A versus CS. Thus, the presence of açai extract in cigarettes had a protective effect against emphysema in mice, probably by reducing oxidative and inflammatory reactions. These results raise the possibility that addition of açaí extract to normal cigarettes could reduce their harmful effects.

Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide.

Short-term exposure to cigarette smoke (CS) or lipopolysaccharide (LPS) leads to acute lung inflammation through oxidant-antioxidant imbalance. We studied the response in mice exposed to smoke or LPS during five consecutive days, as measured by superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, as well as lipid peroxidation and nitric oxide levels in bronchoalveolar lavage fluid (BALF), lung homogenates, and plasma. Control mice were exposed to ambient air. Exposure to CS or LPS led to a similar influx of alveolar macrophages and neutrophils into the BALF; however, hydroxyproline levels were increased only in the CS group (p<0.001); SOD activity was increased in the BALF (p<0.001) and lung homogenates (p<0.05) of the CS group but was decreased in the BALF (p<0.05), lung homogenates (p<0.05) and plasma (p<0.01) of the LPS group. CAT activity was increased in the BALF (p<0.01), lung homogenates (p<0.001) and plasma (p<0.05) of the CS group but decreased in the BALF (p<0.001) and plasma (p<0.05) of the LPS group. GPx activity was reduced in the BALF (p<0.01) and plasma (p<0.01) of both the CS and LPS groups. Lipid peroxidation was increased in the BALF (p<0.001) and lung homogenates (p<0.001) of the CS group. Finally, the levels of nitrite were reduced in the CS (p<0.01) and LPS (p<0.001) groups. Our data show that the activity profiles of enzymes contributing to oxidant-antioxidant imbalance in the lungs differ depending on the inflammatory stimulus, and that SOD, CAT and GPx may be useful markers of oxidative stress in acute lung inflammation induced by exposure to CS.