期刊文献+

姜黄素对IL-17诱导的人角质形成细胞NO合成以及iNOS表达的影响 被引量:5

Effect of curcumin on IL-17-induced nitric oxide production and expression of iNOS in human keratinocytes
下载PDF
导出
摘要 目的:探讨姜黄素对IL-17诱导的人表皮角质形成细胞株(HaCaT细胞)NO合成以及诱导型一氧化氮合酶(iN-OS)的mRNA和蛋白表达的影响。方法:用IL-17刺激体外培养的HaCaT细胞,并分别加入3种浓度的姜黄素共培养24 h。并收集细胞上清液、提取细胞总RNA、总蛋白,分别进行NO含量的测定、荧光定量PCR和W estern b lot实验,明确姜黄素对NO含量以及iNOS表达的影响。结果:IL-17能够有诱导HaCaT细胞NO以及iNOS的表达(P<0.01)。姜黄素有效下调NO合成量以及iNOS的mRNA(P<0.01)及蛋白表达(P<0.01)水平。结论:姜黄素对IL-17诱导的HaCaT细胞NO分泌及iNOS的表达具有明显的抑制作用,从而为其对角质形成细胞相关的皮肤炎症性疾病的治疗提供了理论依据。 AIM: To investigate the effect of curcumin on IL-17-induced NO production,mRNA and protein expression of iNOS in human keratinocyte cell lines(HaCaT cells).METHODS: HaCaT cells were stimulated with IL-17 and incubated with three doses of curcumin for 24h in vitro.After collections of supernatant,total RNA and protein,NO levels in supernatant were detected and fluorescence quantitative PCR and Western blot were performed to determine the effect of curcumin on NO levels and iNOS.RESULTS: IL-17 increased NO levels,and expression of iNOS in HaCaT cells(P0.01).Curcumin decreased IL-17 induced NO production and the iNOS expression at mRNA(P0.01) and protein(P0.01) levels significantly.CONCLUSION: Curcumin down-regulates IL-17-induced NO secretions and iNOS expression in HaCaT cells,thus provides a theoretical basis for the treatment of inflammatory diseases of skin related to keratinocytes.
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2011年第9期959-961,共3页 Chinese Journal of Cellular and Molecular Immunology
基金 国家自然科学基金资助项目(30371295)
关键词 姜黄素 一氧化氮 诱导型一氧化氮合酶 IL-17 角质形成细胞 curcumin nitric oxide inducible nitric oxide synthase IL-17 keratinocyte
  • 相关文献

参考文献3

  • 1Tokura Y, Moil T, Hino R. Psoriasis and Other Thl7-Mediated Skin Diseases[J]. J UOEH, 2010, 32(4) : 317 -328.
  • 2Tokura Y, Moil T, Hino R. Psoriasis and Other Th17-Mediated Skin Diseases[J]. J UOEH, 2010, 32(4) : 317 -328.
  • 3李家文,陈旭娥,刘志香,岳青,刘厚君.Expression of Th17 Cytokines in Skin Lesions of Patients with Psoriasis[J].Journal of Huazhong University of Science and Technology(Medical Sciences),2007,27(3):330-332. 被引量:10

二级参考文献6

  • 1Aggarwal S,Ghilardi N,Xie M H et al.Interleukin-23 promotes a distinct CD4 T cell activation state character- ized by the production of interleukin-17[].Journal of Biological Chemistry.2003
  • 2Harrington L E,Mangan P R,Weaver C T.Expanding the effector CD4 T-cell repertoire: the Th17 lineage[].Current Opinion in Immunology.2006
  • 3Infante-Duarte C,Horton H F,Byrne M C et al.Micro- bial lipopeptides induce the production of IL-17 in Th cell[].J Immunol.2000
  • 4Iwakura Y,Ishigame H.The IL-23/IL-17 axis in inflam- mation[].The Journal of Clinical Investigation.2006
  • 5Langrish C L,Chen Y,Blumenschein W M et al.IL-23 drives a pathogenic T cell population that induces auto- immune inflammation[].The Journal of Experimental Medicine.2005
  • 6Chen Y,Langrish C L,Mckenzie B et al.Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis[].The Journal of Clinical Investigation.2006

共引文献9

同被引文献25

引证文献5

二级引证文献34

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部