摘要
目的探讨青蒿乙素的抗炎活性及其作用机制。方法采用细菌脂多糖(LPS)诱导小鼠单核巨噬细胞RAW264.7建立炎症反应模型,经青蒿乙素处理后,采用Griess试剂检测NO的含量;采用酶联免疫法(ELISA)检测促炎症因子的水平;采用Western Blot检测炎症相关蛋白及激酶的表达水平。结果青蒿乙素能明显抑制RAW264.7细胞中LPS诱导的NO生成,且呈现剂量依赖性,半数抑制浓度(IC50)为4.72μmol·L^(-1)。同时,青蒿乙素也能明显抑制LPS刺激的RAW264.7细胞中诱导性一氧化氮合酶和环氧化酶2的蛋白表达,并降低肿瘤坏死因子α和白细胞介素6的释放。青蒿乙素还能明显抑制LPS所致的IκBα蛋白降解,但是对LPS诱导的ERK、JNK、p38 MAPK活化无明显抑制作用。结论青蒿乙素对LPS所致的RAW264.7细胞炎症反应具有明显的抑制作用,其抗炎机制可能与减少IκBα蛋白降解,进而抑制核转录因子κB炎症信号通路有关。
OBJECTIVE To investigate anti-inflammatory effects and mechanism of arteannuin B. METHODS RAW264. 7 cells were pretreated with arteannuin B,and then stimulated with 1 μg·mL^(-1) lipopolysaccharide( LPS). Nitric oxide( NO)levels were assessed using Griess reagent. The levels of tumor necrosis factor-α and interleukin-6 were detected by Enzyme linked immunosorbent assay. The expression or activation of inflammation-associated proteins was measured by Immunoblotting.RESULTS Arteannuin B dose-dependently inhibited LPS-induced NO production in RAW264. 7 cells with IC50 of 4. 72 μmol·L^(-1). Furthermore,arteannuin B also significantly inhibited the expression of inducible nitric oxide synthase and cyclooxygenase 2,and decreased the release of TNF-α and IL-6 in LPS-exposed RAW264. 7 cells. Moreover,arteannuin B could block LPS-induced degradation of inhibitor of NF-κB α in RAW264. 7 cells. However,arteannuin B did not significantly influence the activation of ERK,JNK,p38 MAPK in LPS-exposed RAW264. 7 cells. CONCLUSION Arteannuin B showed a potent antiinflammatory effect via the NF-κB signaling pathway.
作者
王晶
徐颖
张庆
WANG Jing;XU Ying;ZHANG Qing(Department of Cardiology,West China Hospital,Sichuan University,Chengdu,Sichuan,610041 P.R.China;Drug Clinical Trial’s Office,West China Second University Hospital,Sichuan University,Chengdu,Sichuan,610041 P.R.China;Hospital of Chengdu University of Traditional Chinese Medicine,Chengdu,Sichuan,610075 P.R.China)
出处
《华西药学杂志》
CAS
CSCD
2021年第1期39-43,共5页
West China Journal of Pharmaceutical Sciences
