黄连碱基于NF-κB信号通道的体外抗炎实验研究  

The anti-inflammatory mechanism of coptisine basing on the signal path of NF-κB in vitro

作　　者：潘晓丽[1] 向晖[1] 谢运飞[1] 熊永爱[1] 

机构地区：[1]成都中医药大学药学院,成都611137

出　　处：《中国抗生素杂志》2013年第12期951-954,959,共5页Chinese Journal of Antibiotics

摘　　要：目的探讨黄连碱体外抗炎作用及其机制。方法采用LPS诱导RAW264.7巨噬细胞建立细胞炎症反应模型,用黄连碱对其进行干预,实验结束后,Western Blot技术检测RAW264.7巨噬细胞p-ERK1/2、IκBα和iNOS蛋白的表达。结果与LPS组比较,黄连碱可显著下调LPS所致炎性RAW264.7巨噬细胞中p-ERK1/2和iNOS蛋白表达(P<0.05);显著升高IκBα蛋白的表达(P<0.05)。结论黄连碱抗炎作用机制与其下调LPS诱导的RAW264.7巨噬细胞ERK1/2蛋白磷酸化水平,减少IκB-α蛋白磷酸化降解和抑制iNOS蛋白表达等环节有关。Objective To explore the anti-inflammatory mechanism of coptisine in vitro. Methods In this study, lipopolysaccharide （LPS）-activated macrophage cells （RAW264.7） was employed as an inflammatory model, and the coptisine was used to intervene. After the experiment, Western Blot was used to detect the protein expression of p-ERK1/2, IlcBa and iNOS. Results Compared with LPS group, the coptisine could significantly decrease the expression of protein p-ERK1/2 and iNOS（P〈0.05）, and significantly increase the expression of protein Ird3a（P〈0.05） Conclusion The anti-inflammatory mechanism of coptisine was due to reduce phosphorylation of ERK1/2 protein, degradation of IwBa protein, expression of iNOS protein and such links in LPS-stimulated RAW264.7 macrophages.

关 键 词：黄连碱 抗炎模型 NF id3信号通道蛋白 

分 类 号：R965[医药卫生—药理学]