Induction of Adhesion Molecule Expression in Co-culture of Human Bronchial Epithelial Cells and Neutrophils Suppressed by Puerarin via Down-regulating p38 Mitogen-Activated Protein Kinase and Nuclear Factor κB Pathways

Objective: In this study, we aimed to investigate the expressions of adhesion molecules on human bronchial epithelial cells and neutrophils in co-culture system, assess the effects of puerarin on suppressing these adhesion molecules expressions, and explore the roles of two crucial signal-transducti...

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Published inChinese journal of integrative medicine Vol. 20; no. 5; pp. 360 - 368
Main Author 刘野 邵玲俐 庞伟 兰晓梅 吕建新 丛玉隆 王成彬
Format Journal Article
LanguageEnglish
Published Heidelberg Chinese Association of Traditional and Western Medicine 01.05.2014
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ISSN1672-0415
1993-0402
1993-0402
DOI10.1007/s11655-013-1515-6

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Summary:Objective: In this study, we aimed to investigate the expressions of adhesion molecules on human bronchial epithelial cells and neutrophils in co-culture system, assess the effects of puerarin on suppressing these adhesion molecules expressions, and explore the roles of two crucial signal-transduction elements p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappa B (NF- K B) in modulating adhesion molecules expressions. Methods: Neutrophils and BEAS-2B cells (one human bronchial epithelial cell line) were co-cultured, and adhesion molecules expressions on cell surface were detected using flow cytometry. The mRNA levels of adhesion molecules were assessed by real-time quantitative polymerase chain reaction (real-time qPCR). Phosphorylated p38 MAPK and inhibitor K B were analyzed by Western blot. Results: In co-culture system, adhesion molecules expressions on BEAS-2B cells and neutrephils were enhanced significantly (P〈0.05). Correspondingly, the mRNA levels of adhesion molecules were also increased greatly. Moreover, the pretreatment of peurarin obviously suppressed adhesion molecules expressions on cell surface. Furthermore, phosphorylated p38 MAPK and inhibitor K B in BEAS-2B cells and neutrophils were elevated in co-culture system, but decreased significantly after upon the treatment of peurarin (P〈0.05). Conclusions: Co- culture boosted the interactions between human bronchial epithelial cells and neutrophils mimicking airway inflammation, whereas peurarin decreased the expression of adhesion molecules on cell surface by suppressing the activities of p38 MAPK and NF- K B pathways, and exhibiting its anti-inflammation activity.
Bibliography:bronchial epithelial cells, neutrophils, puerarin, adhesion molecules, p38 mitogen-activatedprotein kinase, nuclear factor kappa B
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Objective: In this study, we aimed to investigate the expressions of adhesion molecules on human bronchial epithelial cells and neutrophils in co-culture system, assess the effects of puerarin on suppressing these adhesion molecules expressions, and explore the roles of two crucial signal-transduction elements p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappa B (NF- K B) in modulating adhesion molecules expressions. Methods: Neutrophils and BEAS-2B cells (one human bronchial epithelial cell line) were co-cultured, and adhesion molecules expressions on cell surface were detected using flow cytometry. The mRNA levels of adhesion molecules were assessed by real-time quantitative polymerase chain reaction (real-time qPCR). Phosphorylated p38 MAPK and inhibitor K B were analyzed by Western blot. Results: In co-culture system, adhesion molecules expressions on BEAS-2B cells and neutrephils were enhanced significantly (P〈0.05). Correspondingly, the mRNA levels of adhesion molecules were also increased greatly. Moreover, the pretreatment of peurarin obviously suppressed adhesion molecules expressions on cell surface. Furthermore, phosphorylated p38 MAPK and inhibitor K B in BEAS-2B cells and neutrophils were elevated in co-culture system, but decreased significantly after upon the treatment of peurarin (P〈0.05). Conclusions: Co- culture boosted the interactions between human bronchial epithelial cells and neutrophils mimicking airway inflammation, whereas peurarin decreased the expression of adhesion molecules on cell surface by suppressing the activities of p38 MAPK and NF- K B pathways, and exhibiting its anti-inflammation activity.
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ISSN:1672-0415
1993-0402
1993-0402
DOI:10.1007/s11655-013-1515-6