Study of Anti-inflammatory effect by Cucurbitacin E via modulation of PI3K/Akt/NF-κB pathways.
Wenxiang Cheng; Qingyun Jia; Ye Yue; Yingping Hu; Zhanwang Xu; Peng Zhang
2015
会议名称第十七届骨科学术会议暨第十届COA国际学术大会
会议地点重庆
英文摘要Objective: Increasing studies indicate that Cucurbitacin E (CuE), a derivative isolated from Cucurbitaceae plants may exert anti-inflammatory effect. In this study we explore the effect of CuE on TNF-α-induced inflammatory cytokines production in human synoviocytes MH7A cells, and further explore the detailed molecular mechanism involved in its anti-inflammatory effect. Materials and method: MH7A cells were stimulated with TNF-α in the presence or absence of CuE, The expression of pro-inflammatory cytokines was determined by quantitative real-time PCR and enzyme-linked immunosorbent assay (ELISA). Signal-transduction protein expression was determined by Western blot. Nuclear translocation of NF-κB p65 was determined by a confocal fluorescence microscopy. Result: CuE suppresses TNF-α-induced interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-8 (IL-8) mRNA and protein expression in MH7A cells in a dose-dependent manner with no apparent cytotoxicity. CuE also suppressed TNF-α-induced phosphorylation of NF-κB p65, IKKα/β, IκBα as well as NF-κB p65 nuclear translocation in a dose-and time-dependent manner. Furthermore, CuE suppresses the TNF-α-induced activiation of PI3K/Akt similarly as the PI3K inhibitor LY294002,which also decreases the activation of NF-κB as well as mRNA and protein expression of IL-1β, IL-6, and IL-8 in TNF-α-induced MH7A cells. Conclusion: These findings demonstrate that Cucurbitacin E as a potential therapeutic agent for Rheumatoid arthritis can inhibits TNF-α-induced inflammatory cytokine production in human synoviocyte MH7A cells via modulation of PI3K/Akt/NF- κB pathway.
收录类别其他
语种英语
内容类型会议论文
源URL[http://ir.siat.ac.cn:8080/handle/172644/7314]  
专题深圳先进技术研究院_医工所
作者单位2015
推荐引用方式
GB/T 7714
Wenxiang Cheng,Qingyun Jia,Ye Yue,et al. Study of Anti-inflammatory effect by Cucurbitacin E via modulation of PI3K/Akt/NF-κB pathways.[C]. 见:第十七届骨科学术会议暨第十届COA国际学术大会. 重庆.
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