摘要
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.
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.
基金
Supported by the National Natural Sciences Foundation of China(No.30873419)
