Discipline of Pathology, Redox Biology Group and Bosch Institute, The University of Sydney, Sydney, NSW 2006, Australia.
Biochem J. 2011 May 1;435(3):669-77. doi: 10.1042/BJ20101728.
Accumulating Mb (myoglobin) in the kidney following severe burns promotes oxidative damage and inflammation, which leads to acute renal failure. The potential for haem-iron to induce oxidative damage has prompted testing of iron chelators [e.g. DFOB (desferrioxamine B)] as renal protective agents. We compared the ability of DFOB and a DFOB-derivative {DFOB-AdAOH [DFOB-N-(3-hydroxyadamant-1-yl)carboxamide]} to protect renal epithelial cells from Mb insult. Loading kidney-tubule epithelial cells with dihydrorhodamine-123 before exposure to 100 μM Mb increased rhodamine-123 fluorescence relative to controls (absence of Mb), indicating increased oxidative stress. Extracellular Mb elicited a reorganization of the transferrin receptor as assessed by monitoring labelled transferrin uptake with flow cytometry and inverted fluorescence microscopy. Mb stimulated HO-1 (haem oxygenase-1), TNFα (tumour necrosis factor α), and both ICAM (intercellular adhesion molecule) and VCAM (vascular cell adhesion molecule) gene expression and inhibited epithelial monolayer permeability. Pre-treatment with DFOB or DFOB-AdAOH decreased Mb-mediated rhodamine-123 fluorescence, HO-1, ICAM and TNFα gene expression and restored monolayer permeability. MCP-1 (monocyte chemotactic protein 1) secretion increased in cells exposed to Mb-insult and this was abrogated by DFOB or DFOB-AdAOH. Cells treated with DFOB or DFOB-AdAOH alone showed no change in permeability, MCP-1 secretion or HO-1, TNFα, ICAM or VCAM gene expression. Similarly to DFOB, incubation of DFOB-AdAOH with Mb plus H2O2 yielded nitroxide radicals as detected by EPR spectroscopy, indicating a potential antioxidant activity in addition to metal chelation; Fe(III)-loaded DFOB-AdAOH showed no nitroxide radical formation. Overall, the chelators inhibited Mb-induced oxidative stress and inflammation and improved epithelial cell function. DFOB-AdAOH showed similar activity to DFOB, indicating that this novel low-toxicity chelator may protect the kidney after severe burns.
在严重烧伤后,Mb(肌红蛋白)在肾脏中的积累会促进氧化损伤和炎症,从而导致急性肾衰竭。血红素铁诱导氧化损伤的潜力促使人们测试铁螯合剂[例如 DFOB(去铁胺 B)]作为肾脏保护剂。我们比较了 DFOB 和 DFOB 衍生物{DFOB-AdAOH[DFOB-N-(3-羟基金刚烷-1-基)羧酰胺]}保护肾上皮细胞免受 Mb 损伤的能力。在暴露于 100μM Mb 之前,用二氢罗丹明 123 加载肾小管上皮细胞,与对照(无 Mb)相比,罗丹明 123 荧光增加,表明氧化应激增加。通过监测用流式细胞术和倒置荧光显微镜标记的转铁蛋白摄取来评估 Mb 诱导的转铁蛋白受体的重排。Mb 刺激 HO-1(血红素加氧酶-1)、TNFα(肿瘤坏死因子 α)以及 ICAM(细胞间黏附分子)和 VCAM(血管细胞黏附分子)基因的表达,并抑制上皮细胞单层通透性。DFOB 或 DFOB-AdAOH 预处理可降低 Mb 介导的罗丹明 123 荧光、HO-1、ICAM 和 TNFα 基因表达,并恢复单层通透性。暴露于 Mb 损伤的细胞中 MCP-1(单核细胞趋化蛋白 1)分泌增加,DFOB 或 DFOB-AdAOH 可阻断该分泌。单独用 DFOB 或 DFOB-AdAOH 处理的细胞,其通透性、MCP-1 分泌或 HO-1、TNFα、ICAM 或 VCAM 基因表达均无变化。与 DFOB 类似,用 EPR 光谱法检测到 DFOB-AdAOH 与 Mb 和 H2O2 孵育生成了氮氧自由基,表明其除了金属螯合之外还具有潜在的抗氧化活性;负载 Fe(III)的 DFOB-AdAOH 未形成氮氧自由基。总之,螯合剂抑制了 Mb 诱导的氧化应激和炎症,并改善了上皮细胞功能。DFOB-AdAOH 表现出与 DFOB 相似的活性,表明这种新型低毒性螯合剂在严重烧伤后可能会保护肾脏。