白芍总苷对巨噬细胞一氧化氮和诱导型一氧化氮合酶生成的影响及其机制研究  

Effects of total glucosides of paeony on nitric oxide and inducible nitric oxide synthase production in macrophages and its mechanism

作　　者：陈刚[1] 郭莉霞[1] 邓小红[1] 殷忠意[1] 景佳佳[1] 

机构地区：[1]重庆工商大学药物化学与化学生物学研究中心,重庆400067

出　　处：《中国免疫学杂志》2008年第4期345-347,351,共4页Chinese Journal of Immunology

基　　金：重庆市教委科学技术研究项目(KJ060702)

摘　　要：目的:探讨白芍总苷(TGP)抗炎作用与调节巨噬细胞一氧化氮(NO)的产生及诱导型一氧化氮合酶(iNOS)的表达的关系,并从调控核转录因子-κB(NF-κB)活性的途径探讨其作用机制。方法:预先用不同浓度的TGP与大鼠腹腔巨噬细胞共同孵育,然后加入脂多糖(LPS)刺激细胞,检测细胞培养液中NO的产生,Westernblot方法检测iNOS的表达和NF-κB抑制蛋白α(IκBα)的含量,同时检测NF-κB与DNA的结合活性。结果:TGP显著抑制了LPS诱导的大鼠腹腔巨噬细胞产生NO、表达i-NOS,同时也显著增加了细胞内IκBα蛋白的含量和抑制了NF-κB与DNA的结合活性。结论:TGP的抗炎作用与其通过抑制巨噬细胞NF-κB的活性,从而降低巨噬细胞iNOS的表达、减少NO产生密切相关。Objective：To investigate the effects of total glucosides of paeony（TGP） on nitric oxide production（NO） and expression of inducible nitric oxide synthase（iNOS） in macrophages activated by lipopolysaccharides（LPS） and the mechanism involved.Methods：Rat peritoneal macrophages were pre-treated with TGP and then stimulated by LPS.NO production in culture medium was examined.Cellular protein was prepared for the determination of iNOS or nuclear factor-κB（NF-κB） inhibitory κB（IκB） by Western blot analysis.Further,DNA binding activity of NF-κB complex was also analyzed.Results：TGP markedly suppressed LPS-induced NO production and iNOS expression in rat peritoneal macrophages.TGP also significantly increased amounts of IκB protein and inhibited DNA binding activity of NF-κB complex in LPS-stimulated rat peritoneal macrophages.Conclusion：Results of this study suggest that modulation of iNOS and NF-κB may be brought about by TGP,resulting in prevention of inflammation.

关 键 词：白芍总苷 一氧化氮 诱导型一氧化氮合酶 核因子-ΚB 巨噬细胞 

分 类 号：R392[医药卫生—免疫学]