title: Protective effect of genistein on lipopolysaccharide-induced acute lung injury in rats.
abstract: 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 (MPO) 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 1 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.
authors.affiliation: Department of Anesthesiology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical College, Wenzhou, 325027, China.
authors.forename: Xingwang
authors.initials: X
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Xu
authors.forename: Qingquan
authors.initials: Q
authors.lastname: Lian
authors.forename: Bangxiong
authors.initials: B
authors.lastname: Zeng
authors.forename: Bing
authors.initials: B
authors.lastname: Zhang
authors.forename: Yubo
authors.initials: Y
authors.lastname: Xie
mesh_terms: D000818:Animals; D019833:Genistein / Q000494:pharmacology* / Q000627:therapeutic use; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000235:genetics; D008070:Lipopolysaccharides; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012128:Respiratory Distress Syndrome / Q000139:chemically induced / Q000517:prevention & control*
chemical_list: D008070:Lipopolysaccharides; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1; D019833:Genistein