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Phytomedicine 2012-Feb

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

Només els usuaris registrats poden traduir articles
Inicieu sessió / registreu-vos
L'enllaç es desa al porta-retalls
Roberto Soares de Moura
Thiago Santos Ferreira
Alan Aguiar Lopes
Karla Maria Pereira Pires
Renata Tiscoski Nesi
Angela Castro Resende
Pergentino Jose Cunha Souza
Antônio Jorge Ribeiro da Silva
Ricardo Moreira Borges
Luis Cristóvão Porto

Paraules clau

Resum

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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