Protective Effect of Resveratrol on Acute Lung Injury Induced by Lipopolysaccharide in Mice

被引:23
|
作者
Cao, Quan [1 ,2 ]
Jing, Changwen [3 ]
Tang, Xinyi [3 ]
Yin, Ye [3 ]
Han, Xiao [3 ]
Wu, Wenxi [1 ,2 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Gen Surg, Nanjing 210029, Peoples R China
[2] Nanjing Med Univ, Affiliated Hosp 1, Dept ICU, Nanjing 210029, Peoples R China
[3] Nanjing Med Univ, Clin Diabet Ctr Jiangsu Prov, Nanjing 210029, Peoples R China
来源
ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY | 2011年 / 294卷 / 03期
关键词
resveratrol; acute lung injury; lipopolysaccharide; NF-kappa B; NF-KAPPA-B; NITRIC-OXIDE SYNTHASE; RESPIRATORY-DISTRESS-SYNDROME; PULMONARY-EDEMA; INFLAMMATION; INHIBITOR; ACTIVATION; INDUCTION; MORTALITY; PATHWAYS;
D O I
10.1002/ar.21331
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Resveratrol, a phytoalexin found in a range of plant products, may exert a variety of pharmacological activities. In this study, we investigated the effect of resveratrol on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo, and we found that the pretreatment with resveratrol can effectively protect mice against LPS-induced ALI. Mice were pretreated with 1 mg/kg resveratrol for 3 days before challenging with a dose of 15 mg/kg LPS. The histological result showed that resveratrol can suppress the edema, inflammatory cell infiltration, and alveolar structure damage of lungs in ALI mice, and a decrease in the lung W/D ratio was also observed in mice with resveratrol pretreatment. Additionally, resveratrol markedly decreased the production of inflammatory cytokines, including IL-1 beta and MIP-1 alpha and prevented the release of nitric oxide (NO) through inhibiting the expression of inducible NO synthase in lung tissues. Furthermore, the pretreatment with resveratrol suppressed the nuclear translocation of NF-kappa B in lung tissues, which may be partly responsible for its effect on the ALI. In conclusion, the results presented here may suggest resveratrol as a potential therapeutic agent for treating ALI in the future. Anat Rec, 294:527-532, 2011. (C) 2011 Wiley-Liss, Inc.
引用
收藏
页码:527 / 532
页数:6
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