检索结果-南通市图书馆

Inhibition of p38 mitogen-activated protein kinase attenuates experimental autoimmune hepatitis: Involvement of nuclear factor kappa B

引用

World Journal of Gastroenterology 2007年第31期13卷 4249-4254页

作者： Xiong Ma Yi-Tao Jia De-Kai Qiu ShanghaiJiaotong University School of Medicine Shanghai Institute ofDigestive Disease Shanghai 200001 China

To investigate the role of p38 mitogen-activated protein kinase （p38MApK） in murine experimental autoimmune hepatitis （EAH）.METHODS： To induce EAH, the syngeneic S-100 antigen emulsified in complete Freud＇s adjuvant was injected intraperitoneally into adult male C57BI/6 mice. Liver injury was assessed by serum ALT and liver histology. The expression and activity of p38 MApK were measured by Western blot and kinase activity assays. In addition, DNA binding activities of nuclear factor kappa B （NF-KB） were analyzed by electrophoretic mobility shift assay. The effects of SB203580, a specific p38 MApK inhibitor, on liver injuries and expression of proinflammatory cytokines （interferon-y, IL-12, IL-1β and TNF-α） were ***： The activity of p38 MApK and NF-~：B was increased and reached its peak 14 or 21 d after the first syngeneic S-100 administration. Inhibition of p38 MApK activation by SB203580 decreased the activation of NF-~：B and the expression of proinflammatory cytokines. Moreover, hepatic injuries were improved significantly after SB203580 administration.

关键词： Autoimmune hepatitis p38 mitogen-activatedprotein kinase Nuclear factor kappa B proinflammatorycytokines

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

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

引用

Chinese Journal of Integrative Medicine 2014年第5期20卷 360-368页

作者：刘野邵玲俐庞伟兰晓梅吕建新丛玉隆王成彬 Department of Clinical Laboratory Chinese People's Liberation Army General Hospital Deparment of Laboratory Medicine Wenzhou Medical College

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.

关键词： bronchial epithelial cells neutrophils puerarin adhesion molecules p38 mitogen-activatedprotein kinase nuclear factor kappa B

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：