瘦素通过NLRP3炎性体对小鼠骨髓树突状细胞的作用及机制

发布时间：2018-04-22 21:29

本文选题：瘦素 + NLRP炎性体　；参考：《中国免疫学杂志》2017年07期

【摘要】：目的:探讨瘦素通过NLRP3炎性体对树突状细胞的作用及其机制。方法:体外诱导小鼠骨髓来源的树突状细胞(BMDCs),用不同浓度瘦素与BMDCs共同培养,分别检测培养上清IL-1β和IL-18的蛋白和基因水平,用FLICA试剂盒或ROS试剂盒分别在流式细胞仪上检测caspase-1活性或胞内ROS生成情况。瘦素与BMDCs共培养,加入caspase-1抑制剂或用siRNA干扰NLRP3基因表达,检测前后加入IL-1β和IL-18基因和蛋白表达水平。瘦素与BMDCs共培养,加入ROS抑制剂或KCL,检测加入前后IL-1β和IL-18蛋白分泌水平。结果:瘦素促进BMDCs分泌IL-1β和IL-18。瘦素通过上调NLRP3基因促进IL-1β和IL-18基因和蛋白表达,通过激活caspase-1蛋白提高IL-1β基因和蛋白水平,K~+外流参与此过程。结论:瘦素通过激活NLRP3炎性体促进BMDCs IL-1β和IL-18基因和蛋白表达,此过程部分通过K~+外流实现。这提示瘦素可能是NLRP3炎性体的激活剂。
[Abstract]:Objective: To investigate the effect and mechanism of leptin on dendritic cells through NLRP3 inflammatory cells. Methods: dendritic cells (BMDCs) derived from bone marrow of mice were induced in vitro. The protein and gene level of IL-1 beta and IL-18 in supernatant were detected by co culture with different concentrations of leptin and BMDCs, respectively, with FLICA kit or ROS kit in flow cytometry, respectively. Caspase-1 activity or intracellular ROS formation was detected by cytosgraph. Leptin was co cultured with BMDCs, Caspase-1 inhibitor or siRNA interfered with NLRP3 gene expression, IL-1 beta and IL-18 genes and protein expression levels were added before and after detection. Leptin and BMDCs were co cultured, ROS inhibitor or KCL were added to detect the secretion of IL-1 beta and protein. Results: leptin stimulates BMDCs secretion of IL-1 beta and IL-18. leptin to promote the expression of IL-1 beta and IL-18 genes and proteins by up regulation of NLRP3 gene, and improves the level of IL-1 beta gene and protein by activating caspase-1 protein, and K~+ Exodus participates in this process. Conclusion: leptin promotes BMDCs IL-1 beta and gene and protein expression by activating NLRP3 inflammatory bodies. It is partly achieved through the K~+ outflow, suggesting that leptin may be an activator of NLRP3 inflammatory body.

【作者单位】：复旦大学附属华山医院风湿科;上海市血液中心血液工程学科;
【基金】：国家自然科学基金项目(81401345) 复旦大学附属华山医院北院青年医师培养计划资助
【分类号】：R392

【相似文献】