Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells
Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells
复制标题
一氧化碳抑制小鼠肾小管上皮细胞体外氧化应激损伤模型中 HMGB1 的核胞质转位
DOI：
10.1007/s11596-016-1663-y
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发表时间：
2016-12-01
影响因子：
--
通讯作者：
Chen, Gang
中科院分区：
文献类型：
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作者：
Jia, Yu;Wang, Lu;Chen, Gang
一氧化碳（CO）作为信号通路中重要的小分子，参与了肾移植缺血再灌注损伤（IRI）的发生。CO释放分子-2 （CORM-2）是一种CO释放分子，是一种能在体内快速释放CO的金属羰基配合物。本研究建立体外氧化应激损伤模型，研究CORM-2预处理对小鼠原代肾近端小管上皮细胞（RPTECs）高迁移率组盒1蛋白（HMGB1）核质易位的影响。免疫荧光染色显示，HMGB1在培养基和CORM-2处理组中主要定位于细胞核，而在H2O2-和无活性CORM-2 （iCORM-2）处理组中较多的HMGB1易位到细胞质中。HMGB1的Western blotting结果显示，h2o2处理组（0.59 +/- 0.27）和icorm -2处理组（0.57 +/- 0.22）的胞质HMGB1总量显著高于中处理组（0.19 +/- 0.05）和corm -2处理组（0.21 +/- 0.10）（P < 0.05）
Carbon monoxide (CO), as a vital small molecule in signaling pathways, is found to be involved in ischemia-reperfusion injury (IRI) in renal transplantation. CO-releasing molecule-2 (CORM-2), a CO-releasing molecule, is a type of metal carbonyl complexes which can quickly release CO in vivo. In this study, an in vitro oxidative stress injury model was established to examine the effect of CORM-2 pretreatment on the nuclear-cytoplasmic translocation of high mobility group box 1 protein (HMGB1) in mouse primary renal proximal tubular epithelial cells (RPTECs). Immunofluorescence staining showed that HMGB1 in the medium-and CORM-2-treated groups was predominantly localized in the nucleus of the cells, whereas higher amounts of HMGB1 translocated to the cytoplasm in the H2O2- and inactive CORM-2 (iCORM-2)-treated groups. Western blotting of HMGB1 showed that the total amounts of cytoplasmic HMGB1 in the H2O2-treated (0.59 +/- 0.27) and iCORM-2-treated (0.57 +/- 0.22) groups were markedly higher than those in the medium-treated (0.19 +/- 0.05) and CORM-2-treated (0.21 +/- 0.10) groups (P