4.7 Article

Protective effect of quercetin against paraquat-induced lung injury in rats

期刊

LIFE SCIENCES
卷 87, 期 5-6, 页码 181-186

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2010.06.011

关键词

Paraquat; Quercetin; Fibrosis; 4-Hydroxyproline; Oxidative stress

资金

  1. Ministry of Education, Science and Technology (MEST), Korea [20090093533]

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Aims: Paraquat (PQ) is known to induce pulmonary injury via a redox cyclic reaction. The present study was aimed to determine the protective effects of quercetin against PQ-induced pulmonary injury in association with its antioxidant activity. Main methods: Male rats were challenged acutely by PQ (50 mg/kg, i.p.) with or without quercetin post-treatment. Pulmonary heme oxygenase-1 (HO-1) expression, malondialdehyde (MDA) level, and the total oxyradical scavenging capacity (TOSC) toward hydroxyl, peroxyl radicals and peroxynitrite were measured 24 h after PQ treatment Different groups of rats were instilled with PQ (0.5 mg/kg) directly into the right lung. Quercetin was administered to the rats daily for 14 days after PQ instillation. Serum NO, pulmonary glutathione (GSH) and 4-hydroxyproline (4-HP) concentrations were quantified in conjunction with histopathological examination to determine the fibrotic changes in lung. Key findings: Pulmonary MDA level and HO-1 expression were elevated and the TOSC was reduced rapidly by an intraperitoneal dose of PQ These changes were inhibited by quercetin post-treatment In rat lungs instilled with PQ 14 days before, NO, MDA and 4-HP were elevated, and GSH was reduced, which were all inhibited significantly by daily quercetin treatment. Histopathological examination also revealed that quercetin ameliorated the increase in fibroblast distribution and collagen deposition in the lungs instilled with PQ. Significance: The present results demonstrate that quercetin administration to rats effectively inhibits the development of PQ-induced pulmonary injury most probably via its antioxidant activity. (C) 2010 Elsevier Inc. All rights reserved.

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