The prevention of oxyhemoglobin-induced endothelial and smooth muscle cytoskeletal injury by deferoxamine.
The prevention of oxyhemoglobin-induced endothelial and smooth muscle cytoskeletal injury by deferoxamine.
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DOI：
10.1227/00006123-199301000-00009
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发表时间：
1993
期刊：
影响因子：
4.8
通讯作者：
Youssef G. Comair;Youssef G. Comair;Hyman M. Schipper;Steven Brem;Steven Brem
中科院分区：
文献类型：
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作者：
Youssef G. Comair;Youssef G. Comair;Hyman M. Schipper;Steven Brem;Steven Brem
血红蛋白的氧化分解产物在脑血管痉挛的发病机制中很重要，因为它们对动脉壁的内皮和平滑肌有影响。培养的血管细胞的细胞骨架变化是氧化损伤的敏感指标。当暴露于 10(-5) M 氧合血红蛋白时，培养的内皮细胞和平滑肌细胞显示出与剂量相关的细胞骨架破坏，特别是 F-肌动蛋白和波形蛋白丝。添加10(-3)M去铁胺或1%白蛋白可防止细胞骨架损伤。这些实验支持去铁胺在血管痉挛的药物治疗中的作用。此外，培养的动脉内皮细胞和平滑肌细胞的细胞骨架研究提供了一种新的体外方法，用于研究血红蛋白分解产物引发的氧化损伤的细胞机制。
The oxidized breakdown products of hemoglobin are important in the pathogenesis of cerebral vasospasm because of their effects on the endothelium and the smooth muscle of the arterial wall. Cytoskeletal changes in cultured vascular cells are sensitive indicators of oxidative injury. Cultured endothelial cells and smooth muscle cells showed a dose-related disruption of the cytoskeleton, particularly the F-actin and vimentin filaments, when exposed to 10(-5) M oxyhemoglobin. The cytoskeletal injury was prevented by the addition of 10(-3) M deferoxamine or 1% albumin. These experiments support a role for deferoxamine in the pharmacological treatment of vasospasm. Furthermore, cytoskeletal studies of cultured arterial endothelial and smooth muscle cells provide a novel in vitro approach by which to study the cellular mechanisms of oxidant injury initiated by the breakdown products of hemoglobin.