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题名: Isoforskolin pretreatment attenuates lipopolysaccharide-induced acute lung injury in animal models
作者: Yang, Weimin1; Qiang, Dongjin1; Zhang, Min1; Ma, Limei1; Zhang, Yonghui1; Qing, Chen1; Xu, Yunlong2; Zhen, Chunlan1; Liu, Jikai2; Chen, Yan-Hua3
刊名: INTERNATIONAL IMMUNOPHARMACOLOGY
关键词: Acute lung injury ; Isoforskolin ; Lipopolysaccharide ; Inflammation ; Cytokine
英文摘要: Isoforskolin was isolated from Coleus forskohlii native to Yunnan in China. We hypothesize that isuforskolin pretreatment attenuates acute lung injury induced by lipopolysaccharide (endotoxin). Three acute lung injury models were used: situ perfused rat lung, rat and mouse models of endotoxic shock. Additionally, lipopolysaccharide stimulated proinflammatory cytokine production was evaluated in human mononuclear leukocyte. In situ perfused rat lungs, pre-perfusion with isoforskolin (100, and 200 mu M) and dexarrethasone (65 mu M, positive control) inhibited lipopolysaccharide (10 mg/L) induced increases in lung neutrophil adhesion rate, myeloperoxidase activity, lung weight Wet/Dry ratio, permeability-surface area product value, and tumor necrosis factor (TNF)-alpha levels. In rats, pretreatments with isoforskolin (5, 10, and 20 mg/kg, i.p.) and dexamethasone (5 mg/kg, i.p.) markedly reduced lipopolysaccharide (6 mg/kg i.v.) induced increases of karyocyte, neutrophil counts and protein content in bronchoalveolar lavage fluid, and plasma myeloperoxidase activity. Lung histopathology showed that morphologic changes induced by lipopolysaccharide were less pronounced in the isoforskolin and dexamethasone pretreated rats. In mice, 5 mg/kg isoforskolin and dexamethasone caused 100% and 80% survival, respectively, after administration of lipopolysaccharide (62.5 mg/kg, iv., 40% survival if untreated). In human mononuclear leukocyte, isoforskolin (50, 100, and 200 mu M) and dexamethasone (10 mu M) pre-incubation lowered lipopolysaccharide (2 mu g/mL) induced secretion of the cytokine TNF-alpha, and interleukins (IL)-1 beta, IL-6, and IL-8. In conclusion, pretreatment with isoforskolin attenuates lipopolysaccharide-induced acute lung injury in several models, and it is involved in down-regulation of inflammatory responses and proinflammatory cytokines TNF-alpha, IL-1 beta, IL-6, and IL-8. (C) 2011 Elsevier B.V. All rights reserved.
出版日期: 2011-06-01
卷号: 11, 期号:6, 页码:683-692
DOI标识: 10.1016/j.intimp.2011.01.011
语种: 英语
ISSN号: 1567-5769
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内容类型: 期刊论文
URI标识: http://ir.kib.ac.cn/handle/151853/5353
Appears in Collections:植物化学与西部植物资源持续利用国家重点实验室_期刊论文

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作者单位: 1.Kunming Med Coll, Yunnan Key Lab Pharmacol Nat Prod, Kunming 650031, Peoples R China
2.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources W China, Kunming 650204, Peoples R China
3.E Carolina Univ, Brody Sch Med, Dept Anat & Cell Biol, Greenville, NC 27834 USA

Recommended Citation:
Yang, WM; Qiang, DJ; Zhang, M; Ma, LM; Zhang, YH; Qing, C; Xu, YL; Zhen, CL; Liu, JK; Chen, YH.Isoforskolin pretreatment attenuates lipopolysaccharide-induced acute lung injury in animal models,INTERNATIONAL IMMUNOPHARMACOLOGY,2011,11(6):683-692
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