抑制剂Rottlerin对巨噬细胞在结核分枝杆菌刺激下NO和TNF分泌的影响  

Rottlerin inhibits mycobacterium tuberulosis induced NO and TNF production by macrophages

作　　者：李珣[1] 黄朝阳[1] 赵元勋[1] 

机构地区：[1]厦门大学附属第一医院检验科,厦门361003

出　　处：《福建医药杂志》2014年第6期1-3,共3页Fujian Medical Journal

基　　金：国家自然科学基金资助项目(81302529);福建省自然科学基金资助项目(2014D007)

摘　　要：目的研究蛋白激酶C-δ在巨噬细胞识别结核分枝杆菌后产生免疫应答过程中的作用,探讨固有免疫抗结核的分子机制。方法用蛋白酶抑制剂预处理体外培养的小鼠巨噬细胞,通过Western Blot分析相关蛋白的表达及磷酸化水平,利用Griess法和ELISA方法检测巨噬细胞在结核分枝杆菌索状因子合成类似物TDB的刺激下释放一氧化氮(NO)和分泌肿瘤坏死因子(TNF)的水平。结果 Syk抑制剂Piceatannol能抑制TDB诱导的PKC-δ磷酸化;经过蛋白激酶C-δ抑制剂Rottlerin的处理,巨噬细胞受TDB诱导释放的NO浓度由对照组的30μM降至5μM,分泌的TNF浓度为对照组的10%。结论蛋白激酶C-δ抑制剂Rottlerin抑制TDB诱导的巨噬细胞释放NO和分泌TNF,提示PKC-δ在抗结核固有免疫中发挥重要的作用。Objective To study the role of protein kinase C-δin innate immunity against mycobacterium tuberculosis（MTB）.Methods Mouse bone marrow derived macrophages were pre-incubated with different protein kinase inhibitors and then stimulated with MTB cord factor analogue trehalose dibehenate（TDB）.The phosphorylation of related proteins was determined by Western Blot.Nitric oxide produced and TNF released by macrophages were measured with Griess reaction and ELISA,respectively.Results Syk inhibitor Piceatannol reduced TDB induced PKC-δphosphorylation.After incubation with Rottlerin,NO produced by macrophages decreased from 30μM to 5μM and TNF release became 10% of control.ConclusionPKC-δinhibitor Rottlerin reduced production of TDB induced nitric oxide and release of TNF by macrophages.It suggests that PKC-δplays an important role in innate immunity against MTB.

关 键 词：蛋白激酶C-δ 巨噬细胞 结核分枝杆菌 

分 类 号：R378.911[医药卫生—病原生物学]