Protective Effect of Genistein on Lipopolysaccharide-induced Acute Lung Injury in Rats

Summary: To investigate the protective effect of genistein on endotoxin-induced acute lung injury in rats, and explore the underlying mechanisms, 32 male Sprague-Dawley rats were randomly divided into 4 experimental groups: saline control, genistein alone, lipopolysaccaride alone, and genistein pret...

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Published inJournal of Huazhong University of Science and Technology. Medical sciences Vol. 25; no. 4; pp. 454 - 457
Main Author 李兴旺 徐涛 连庆泉 曾邦雄 张冰 谢玉波
Format Journal Article
LanguageEnglish
Published China Department of Anesthesiology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical College, Wenzhou , 325027, China%Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 2005
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ISSN1672-0733
1993-1352
DOI10.1007/BF02828222

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Summary:Summary: To investigate the protective effect of genistein on endotoxin-induced acute lung injury in rats, and explore the underlying mechanisms, 32 male Sprague-Dawley rats were randomly divided into 4 experimental groups: saline control, genistein alone, lipopolysaccaride alone, and genistein pretreatment. Each treatment group consisted of eight animals. Animals were observed for 6 h after LPS challenge, and the wet/dry (W/D) weight ratio of the lung and bronchoalveolar lavage fluid (BALF) protein content were used as a measure of lung injury. Neutrophil recruitment and activation were evaluated by BALF cellularity and myeloperoxidase (MP()) activity. RT-PCR analysis was performed in lung tissue to assess gene expression of ICAM-1. The histopathological changes were also observed using the HE staining of lung tissue. Our results showed that lung injury parameters, including the wet/dry weight ratio and protein content in BALF, were significantly higher in the LPS alone group than in the saline control group (P〈0.01). In the LPS alone group, a larger number of neutrophils and greater MPO activity in cell-free BAL and lung homogenates were observed when compared with the saline control group (P〈0.01). There was a significant increase in lung ICAM-1 mRNA in response to LPS challenge (P〈0. 01, group L versus group S). Genistein pretreatment significantly attenuated LPS-induced changes in these indices. LPS caused extensive lung damage, which was also lessened after genistein pretreatment. All above-mentioned parameters in the genistein alone group were not significantly different from those of the saline control group. It is concluded that genistein pretreatment attenuated LPS-induced lung injury in rats. This beneficial effect of genistein may involves, in part, an inhibition of neutrophilic recruitment and activity, possibly through an inhibition of lung ICAM-1 expression.
Bibliography:42-1679/R
R563
ICAM-1
lipopolysaccharide
acute lung injury
neutrophils
acute lung injury; lipopolysaccharide; neutrophils; ICAM-1
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1672-0733
1993-1352
DOI:10.1007/BF02828222