摘要
目的:观察黄芪注射液对脂多糖(LPS)诱导的内皮细胞炎症因子产生的影响,并初步探讨黄芪注射液的抗炎作用机制。方法:体外培养的人脐静脉内皮细胞(HUVECs),待细胞生长到融合状态时加入不同浓度(10、20、40 mg/L)的黄芪注射液预处理2 h,然后加入LPS(1 mg/L)作用24 h。用四唑盐比色实验(MTT)检测细胞活力;半定量逆转录-聚合酶链式反应(RT-PCR)和酶联免疫吸附法(ELISA)分别检测内皮细胞细胞间黏附分子-1(ICAM-1)、白介素-8(IL-8)和肿瘤坏死因子-α(TNF-α)mRNA的表达和其在上清液中的含量;实时荧光定量PCR(real-time PCR)检测Toll样受体4(TLR4)mRNA的表达;凝胶电泳迁移率实验(EMSA)检测NF-κB活性。结果:LPS能明显降低细胞活力,并能显著增加ICAM-1I、L-8和TNF-αmRNA的表达和含量,同时TLR4 mRNA的表达和NF-κB的活性也显著升高,而预先应用不同浓度的黄芪注射液处理后,上述效应明显减弱。结论:黄芪注射液抑制炎症因子的产生可能与其抑制TLR-4/NF-κB信号通路有关。
AIM：To observe the effect of radix astragali injection on the production of inflammatory factors induced by lipopolysaccharide（LPS） and investigate the anti-inflammation mechanism of radix astragali injection. METHODS： The human umbilical vein endothelial cells（HUVECs） were treated with LPS（1 mg/L） for 24 h following pretreatment with various concentrations of radix astragali injection（10,20 or 40 mg/L） for 2 h.Cell viability was detected by MTT;The mRNA expression and levels of intercellular adhesion molecule-1（ICAM-1）,interleukin-8（IL-8） and tumor necrosis factor-α（TNF-α） were determinded by reverse transcription-polymerase chain reaction（RT-PCR） and enzyme-linked immunosorbent assay（ELISA） respectively;The mRNA expression of Toll-like receptor 4（TLR4） was measured by real-time quantitative reverse transcription-polymerase chain reaction（real-time RT-PCR） and the activity of nuclear factor kappa B（NF-κB） was assayed by electrotracellular mobility shift assay（EMSA）.RESULTS：LPS could significantly decrease the cell viability,increase the mRNA expression and levels of ICAM-1,IL-8 and TNF-α,upregulate the expression of TLR4 mRNA and NF-κB acitivity.However,the aboving effects of LPS were markedly inhibited by pretreatment with radix astragali injection.CONCLUSION： Radix astragali injection inhibits the production of inflammatory factors may be associated with depressing the TLR4/ NF-κB signaling pathway.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2011年第6期611-616,共6页
Chinese Journal of Clinical Pharmacology and Therapeutics
关键词
黄芪注射液
脂多糖
内皮细胞
TOLL样受体4
核因子-ΚB
炎症因子
Radix astragali injection
Lipopolysaccharide
Endothelial cell
Toll-like receptors 4
Nuclear factor-κB
Inflammatory factor
