白杨素通过MAPK信号抑制LPS诱导的RAW 264.7细胞炎症  

Chrysin inhibiting LPS-induced inflammation of RAW 264.7 cells via MAPK signaling pathway

作　　者：李强[1,2] 齐世美[1] 姜琦 戚之琳[1] 章尧[1] LI Qiang;QI Shimei;JIANG Qi;QI Zhilin;ZHANG Yao(Department of Biochemistry,Wannan Medical College,Wuhu 241002,China)

机构地区：[1]皖南医学院生物化学与分子生物学教研室,安徽芜湖241002 [2]皖南医学院人体解剖学教研室,安徽芜湖241002

出　　处：《皖南医学院学报》2018年第5期409-412,共4页Journal of Wannan Medical College

基　　金：安徽省自然科学基金面上项目(1508085MH149);活性生物大分子研究安徽省重点实验室项目(1306C083008);皖南医学院重点科研项目(WK2017Z07)

摘　　要：目的:探讨白杨素抑制LPS诱导的RAW 264.7细胞炎症的分子机制。方法:用不同浓度的白杨素处理RAW 264.7细胞24 h后,CCK-8法检测细胞活力; western blot检测白杨素对LPS诱导的RAW 264.7细胞中MAPK信号蛋白p-ERK、p-JNK和p-P38水平; ELISA法检测TNF-α、IL-6和NO浓度;活性氧探针检测细胞内ROS释放情况。结果:白杨素浓度低于60 mg/L对RAW 264.7细胞增殖无影响; western blot检测表明白杨素抑制了MAPK信号分子p-ERK、p-JNK和p-P38的水平; ELISA结果显示,白杨素抑制TNF-α、IL-6和NO的释放;此外,白杨素也降低了细胞内ROS的产生。结论:白杨素抑制LPS诱导的RAW 264.7细胞炎症反应是通过MAPK信号实现的。Objective ：To investigate the anti-inflammatory mechanisms of chry-sin in RAW 264.7 cells treated with lipopolysaccharides（LPS）. Methods： RAW 264.7 cells were pretreated with different concentration of chrysin for 24 h. Cell viability was determined using CCK-8 kit. The protein levels in MAPK signaling pathway,including p-ERK,p-JNK, and p-P38 were also assessed by western blot. ELISA was performed to detect the concentration of TNF-α, IL-6 and NO in the cellular supematant, lntmcellular level of reactive oxygen species （ROS） was measured using ROS probe. Results：The was no effect on the viability of RAW 264.7 cells under the chrysin（ 60 mg/L） .western blot indicated that chrysin had inhibited the protein levels of MAPK signa- ling molecules,including p-ERK, p-JNK, and p-P38. ELISA showed inhibited release of TNF-α, IL-6 and NO as well as decreased production of intracellular ROS. Conclusion：Anti-inflammatory- mechanism of chrysin in RAW 264.7 cells induced by LPS is achieved via activating MAPK signaling pathway.

关 键 词：白杨素 脂多糖 活性氧簇 RAW 264.7细胞 MAPK信号通路 

分 类 号：R285.5[医药卫生—中药学]