Gelsolin Inhibits the Inflammatory Process Induced by LPS
Gelsolin Inhibits the Inflammatory Process Induced by LPS
复制标题
凝溶胶蛋白抑制 LPS 诱导的炎症过程
DOI：
10.1159/000456043
复制
发表时间：
2017-01-01
影响因子：
--
通讯作者：
Min, Rui
中科院分区：
文献类型：
--
作者：
Cheng, Ying;Hu, Xuguang;Min, Rui
背景/目的：内毒素血症是一种危及生命的情况，是重症监护医学领域的一个关键挑战。巨噬细胞产生的促炎介质在内毒素血症中起关键作用。凝溶胶蛋白（GSN）参与炎症过程。方法：采用ELISA试剂盒测定培养上清中IL-6和TNF-α的含量。通过用Griess测定法测量亚硝酸盐浓度来评估NO产生。通过Lipofectamine转染针对GSN的si-RNA（si-GSN）。结果：LPS可降低GSN水平。重组GSN可抑制LPS诱导的细胞因子并挽救LPS诱导的小鼠死亡，而si-GSN可增加LPS预处理小鼠的死亡。结论：GSN对内毒素血症具有保护作用。
Background/Aims: Endotoxemia is a life-threatening situation that signifies a key challenge in the field of intensive care medicine. Proinflammatory mediators produced by macrophages play a key role in endotoxemia. Gelsolin (GSN) is involved in the process of inflammation. Methods: IL-6 and TNF-α in the supernatant were measured with an ELISA kit. NO production was assessed by measurement of nitrite concentration with the Griess assay. si-RNA directed against GSN (si-GSN) was transfected by Lipofectamine. Results: LPS decreased the levels of GSN. Recombinant GSN inhibited the cytokines induced by LPS and rescued mice from LPS-induced death, and si-GSN increased death in the LPS-pretreated mice. Conclusion: GSN exhibited a protective role in endotoxemia.