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Effects of salidroside on the secretion of inflammatory mediators induced by lipopolysaccharide in murine macrophage cell line J774.1
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- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 1
- DOI:
- 10.13294/j.aps.2016.0096
- Key Word:
- 红景天苷;脂多糖;巨噬细胞;炎症介质;salidroside;lipopolysaccharide;macrophage;inflammatory mediator
Abstract： 本文旨在探讨红景天苷(salidroside,Sal)对脂多糖(lipopolysaccharide,LPS)诱导小鼠巨噬细胞系J774.1炎性活化的影响及其可能机制.J774.1细胞分为PBS对照组、LPS (0.5 μg/mL)刺激组和不同剂量(5、25、125 μg/mL)Sal预处理+LPS组.CCK-8比色法检测细胞活性,ELISA测定培养上清中TNF-α、MCP-1和MIP-2含量,硝酸还原酶法测定上清中NO含量,RT-PCR检测细胞iNOS mRNA表达,Western blot检测胞浆iNOS蛋白和胞浆与胞核NF-KB/p65蛋白表达,TransAMTM NF-κB/p65活性检测试剂盒测定NF-κB/p65 DNA结合活性.结果显示,0.5 μg/mL LPS以及不同剂量(5、25、125μg/mL) Sal处理细胞12 h对J774.1细胞活力无影响;与LPS刺激组比较,LPS刺激前Sal预处理J774.1细胞,培养上清中TNF-α、MCP-1、MIP-2和NO含量呈剂量依赖性降低(P＜0.05),细胞iNOS mRNA和蛋白表达水平下调(P＜0.05),胞核NF-κB/p65蛋白表达降低(P＜0.05)而胞浆NF-κB/p65蛋白相应增加(P＜0.05),且NF-κB/p65 DNA结合活性呈剂量依赖性降低(P＜0.05).以上结果提示,Sal预处理能够降低LPS诱导的巨噬细胞炎性活化,其机制可能通过干扰LPS/TLR4/NF-κB信号通路,从而降低炎性介质及细胞因子的过度表达和分泌.
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