热休克蛋白参与NF-κB介导的H_2O_2预处理的细胞保护作用  

Heat shock proteins were involved in the adaptive cytoprotection of H_2O_2 preconditioning mediated by nuclear factor-κB

作　　者：张梅[1] 郭瑞鲜[2] 莫利球[3] 崔宇[2] 刘微[2] 陈培熹[2] 冯鉴强[2] 

机构地区：[1]广州医学院广州蛇毒研究所,广东广州510082 [2]中山大学中山医学院生理教研室,广州510080 [3]中山大学附属第一医院麻醉科,广州510080

出　　处：《解剖学研究》2007年第6期420-424,共5页Anatomy Research

基　　金：广东省科技计划项目(2006B36004022)

摘　　要：目的探讨热休克蛋白(HSP)是否参与核因子-κB(NF-κB)介导的H2O2预处理的细胞保护作用。方法应用碘化丙啶(PI)染色流式细胞技术(FCM)检测细胞凋亡率,免疫印迹法(Westernblot)测定NF-κB的表达水平,免疫细胞化学染色法测定NF-κB的核转移。结果100μmol/LH2O2预处理PC12细胞90min可显著地抑制300μmol/LH2O2引起的细胞凋亡,并可明显地上调PC12细胞NF-κB的表达及促进NF-κB的核转移,同时也能上调HSP70和HSP90的表达。NF-κB的抑制剂TPCK阻断NF-κB表达,并显著地阻断H2O2预处理的细胞保护作用及HSP70和HSP90的表达。结论HSP70和HSP90参与NF-κB介导的H2O2预处理的适应性细胞保护作用。Objective To investigate whether heat shock proteins （HSPs） were involved in the cytoprotection of H2O2 preconditioning mediated by Nuclear factor-κB （NF-κB）. Methods The percent of apoptotic cells was measured by propidium iodide stain flow cytometry （FCM）, the level of NF-κB expression was detected by Western blot assay, and the nuclear translocation of NF-κB p65 was assessed by immuno-cytochemical staining. Results The preconditioning of H2O2 at 100 μM markedly reduced PC 12 cells apoptosis induced by 300 μmol/L H2O2, and significantly enhanced expression and nuclear translocation of NF-κB p65. Furthermore, 100 μmol/L H2O2 preconditioning also up-regnlated expression of HSP70 and HSP90. N-tosyl-L-phenylalanine chloromethyl ketone （TPCK）, an inhibitor of NF-κB blocked the overexpression of NF-κB, HSP70 and HSP90 induced by H2O2 preconditioning, accompanied with attenuation of H2O2 preconditioning-induced cytoprotectioin. Conclusion HSP70 and HSP90 participated in the adaptive cytoprotection of H2O2 preconditioning mediated by NF-κB pathway.

关 键 词：热休克蛋白 过氧化氢 预处理 核因子-κB 细胞保护 

分 类 号：R363[医药卫生—病理学]