文章摘要
周超 王璞 黄燚 王晗 吴越 高采平 李良平.乳酸杆菌脂磷壁酸抑制脂多糖诱导的大鼠肝脏Kupffer 细胞TLR4 通路 的激活[J].,2015,15(21):4009-4013
乳酸杆菌脂磷壁酸抑制脂多糖诱导的大鼠肝脏Kupffer 细胞TLR4 通路 的激活
Lipoteichoic Acid of LactobacillusBulgaricus Inhibits theLipopolysaccharide-activated TLR4 Pathway in Rat Kupffer Cells
  
DOI:
中文关键词: Kupffer 细胞  Toll 样受体4  乳酸杆菌  脂磷壁酸
英文关键词: Kupffer cells  Toll-like receptor 4  Lipoteichoic Acid
基金项目:四川省卫生厅资助项目(100496)
作者单位
周超 王璞 黄燚 王晗 吴越 高采平 李良平 四川省人民医院消化内科四川省人民医院检验科 
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中文摘要:
      目的:探讨保加利亚乳酸杆菌脂磷壁酸(Lipoteichoic Acid of ,LBG-LTA)对大鼠肝脏Kupffer细胞 Toll样受体4(Toll-like receptor 4,TLR4)信号通路的作用。方法:雄性健康Wistar大鼠10 只(2 月龄,体重250~300 g)处死后,分 离培养肝脏Kupffer 细胞;培养LBG,并提取制备LBG-LTA;Kupffer 细胞,在有或无LBG-LTA(0.1、1、10 ug/mL)预处理的情况 下,给予脂多糖(lipopolysaccharide,LPS,1 EU/mL)刺激后,Western blot 检测各孔Kupffer细胞的TLR4、TANK 结合激酶1(TANK binding kinase-1,TBK1)及核中的核因子B(nuclear factor-kB,NF-kB)水平,酶联免疫吸附法检测各孔培养上清中的肿瘤坏死因子 alpha(tumor necrosis factor-alpha,TNF-alpha)和白介素1beta(interleukin-1beta,IL-1beta)。结果:分离的Kupffer 细胞经不同浓度LBG-LTA 预处理 后,其在LPS刺激下所表达的TLR4、TBK1、核中NF- kB的水平及生成的TNF-alpha和IL-1茁明显低于无LBG-LTA预处理情况下的 LPS 孔(P<0.05),且LBG-LTA 的作用呈浓度依赖性。结论:LBG-LTA以浓度依赖的方式抑制了LPS 诱导下大鼠Kupffer细胞 TLR4 通路的激活。
英文摘要:
      Objective:To determine whether Lipoteichoic Acid of (LBG-LTA) inhibits Toll-like receptor 4 (TLR4) pathway in Kupffer cells isolated from rats.Methods:Ten healthy male Wistar rats, 2 months old, 250~300 g, were killed for the isolation of Kupffer cells. Isolated Kupffer cells were treated with lipopolysaccharide (LPS, 1 EU/mL) with or without LBG-LTA (0.1, 1 or 10 ug/mL) pretreatment. The expression of TLR4, TANK binding kinase-1 (TBK1) and activated nuclear factor-kB (NF- B) in Kupffer cells was measured by Western blot. The production of tumor necrosis factor-alpha(TNF-alpha) and interleukin-1beta(IL-1beta) was quantified by ELISA.Results:The LPS-induced expression of TLR4, TBK1 and activated NF- B and production of TNF-alpha and IL-1beta in isolated Kupffer cells were significantly inhibited by LBG-LTA pretreatment in a dose-dependent manner (P<0.05).Conclusion:LBG-LTA inhibits LPS-activated TLR4 pathway in Kupffer cells of rats in a dose-dependent manner.
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