摘要
旨在证明α-倒捻子素可以缓解脂多糖(LPS)诱导的IEC-6细胞的炎症并揭示其机制。笔者在体外培养的IEC-6细胞中构建LPS诱导的炎症模型,并通过流式细胞术、酶联免疫吸附测定(ELISA)、定量PCR(Q-PCR)、蛋白印迹(Western blot)的方法检测α-倒捻子素对LPS诱导的炎症是否有缓解作用。结果表明,5μmol·L-1的α-倒捻子素预处理可以显著降低LPS诱导的前列腺素E2(PGE2)、白细胞介素-1β(IL-1β)、IL-6和肿瘤坏死因子-α(TNF-α)在IEC-6细胞中的分泌,以及环氧合酶2(COX-2)、IL-6、TNF-α、IL-1βmRNA的表达(P<0.05)。通过对炎症相关信号通路NF-κB的探究可见,α-倒捻子素能显著抑制Toll样受体4(TLR4)mRNA和NF-κB相关蛋白磷酸化IκBα(pIκBα)和磷酸化p65(pp65)的激活(P<0.05)。综上所述,α-倒捻子素可以通过TLR4/NF-κB信号通路来抑制LPS诱导的IEC-6细胞的炎症,并且可能是治疗炎症疾病的潜在选择。
The aim of this study was to prove that α-mangostin can alleviate the lipopolysaccharide(LPS)-induced inflammation of IEC-6 cells and reveal its mechanism.In this study,we constructed an LPS-induced inflammation model in IEC-6 cells in vitro,and examined whether LPS-induced inflammation was reduced by α-mangostin by means of the methods of rheumatology,ELISA,Q-PCR,and Western blot.The results showed that pretreatment with 5 μmol·L^-1 α-mangostin significantly reduced the secretion of prostaglandin(PG)E2,interleukin(IL)-1β,IL-6,tumor necrosis factor(TNF)-α and the expression of COX-2,IL-6,TNF-α,IL-1β mRNA induced by LPS in IEC-6 cells(P<0.05).By investigating the inflammatory-related signaling pathway,NF-κB,we found that α-mangostin significantly inhibited the activation of TLR4 mRNA and NF-κB-related protein phosphorylated IκBα(pIκBα)and phosphorylated p65(pp65)(P<0.05).In summary,α-mangostin can inhibit LPS-induced inflammation of IEC-6 cells through the TLR4/NF-κB signaling pathway and may be a potential treatment for inflammatory diseases.
作者
邹闻书
尹朋
金娜
高倩
刘凤华
ZOU Wenshu;YIN Peng;JIN Na;GAO Qian;LIU Fenghua(Animal Science and Technology College,Beijing University of Agriculture,Beijing 102206,China;Institute of Microbiology,Chinese Academy of Sciences,Beijing 100101,China)
出处
《畜牧兽医学报》
CAS
CSCD
北大核心
2019年第2期431-438,共8页
ACTA VETERINARIA ET ZOOTECHNICA SINICA
基金
北京市科技计划课题(D171100002117002)
