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作 者:王玉刚[1] 吴昊[1] 孟甄[1] 兰嘉琦[1] 游雪甫[2] 邢东明[1] 杜力军[1]
机构地区:[1]清华大学生物科学与技术系药物药理研究室,北京100084 [2]中国医学科学院北京协和医学院医药生物技术研究所,北京100050
出 处:《中国药理学通报》2009年第7期866-870,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No90713043;30801523);清华大学基础研究基金资助项目(No03fd28)
摘 要:目的观察黄芩总黄酮对金葡菌感染后肺脏模式识别受体TLRs和Nods及其相关炎性因子表达的作用,探讨其抗炎药理可能的作用靶点和机制。方法通过构建体外金葡菌感染鼠肺上皮细胞和体内金葡菌急性小鼠肺感染模型,利用RT-PCR技术,通过多种给药形式观察TLR2/Nod2和下游相关炎性因子的mRNA的表达,金葡菌的增殖数量,以探讨其可能的作用靶点和机制。结果黄芩总黄酮不能减少侵入到胞内的活菌数目,但可以下调由于金葡菌侵入导致的TNF-α的大量合成。金葡菌侵入后Nod2表达大幅升高,黄芩总黄酮有明显的抑制作用,并且和TNF-α的变化呈现一定的相关性。TLR2/MyD88的表达无变化。结论黄芩总黄酮的抗炎作用可能与其下调Nod2受体表达进而抑制下游炎性因子表达相关。Aim To explore the anti-inflammation effect of total flavonoids of Radix Scutellariae ( FRS ) , containing of baicalin the principle active component, in vitro and in vivo, and to explore the mechanisms and possible target of FRS action. Methods Depending upon the models of AT 11 (primary alveolar epithelial cells) , in vitro, and the pneumonia mice, in vivo, infected by Staphylococcus aureus, the amount of the bacteria live and mRNA expression of TLR2, Nod2, MyD88 and TNF-α were tested by RT-PCR. Result FRS could not help to reduce the amount of bacteria invaded into the cytoplasm,in vitro and in vivo. It didn' t diminish the rising TNF-α level after the infection caused by Staphylococcus aureus in vitro and in vivo. FRS did not have anti-inflammation effect. TLR2 expression was not changed significantly after the infection and FRS administering. Nod2 expression rose significantly after the infection and was down regulated to near normal after adding FRS. TNF-α and Nod2 showed close correlation. Conclusion The anti-inflammation effect of FRS relies on its ability to repress Nod2 expression.
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