The therapeutic effect of deferoxamine (DFO) for spinal cord injury (SCI) has been demonstrated in previous studies; however, the exact mechanism of action is still unclear. Here, we hypothesized that DFO ameliorates spinal cord compression by promoting neovascularization. Using an SCI model of moderate compression, rats were intraperitoneally injected with 30 mg/kg or 100 mg/kg DFO for 1–2 weeks, and significant neovascularization was found in the injured spinal cord, showing overexpression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), and an increase in the number of new blood vessels. In addition, SCI in rats was significantly ameliorated after treatment with DFO, with less motor dysfunction, increased spared neural tissue, and improved electrophysiological conduction. By contrast, the ameliorative effect of DFO on SCI was suppressed when DFO-induced neovascularization was blocked by lenvatinib, a vascular endothelial growth factor receptor inhibitor, further suggesting that the primary pharmacological effect of DFO in SCI is the promotion of neovascularization. Therefore, we concluded that DFO effectively alleviated SCI by promoting neovascularization in the injured spinal cord. Considering that DFO is an FDA-approved free radical scavenger and iron chelator, it may represent a promising alternative strategy for SCI therapy in the future.

中文翻译：

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去铁胺通过促进大鼠新血管形成改善了压迫性脊髓损伤。

在先前的研究中已经证明了去铁胺（DFO）对脊髓损伤（SCI）的治疗作用。但是，确切的作用机理仍不清楚。在这里，我们假设DFO通过促进新血管形成改善了脊髓压迫。使用中度压迫的SCI模型，大鼠腹膜内注射30 mg / kg或100 mg / kg DFO 1-2周，并且在受伤的脊髓中发现了显着的新生血管形成，表明低氧诱导因子-1α（HIF）过表达-1α）和血管内皮生长因子（VEGF），以及新血管数量增加。此外，用DFO治疗后，大鼠的SCI明显改善，运动功能障碍减少，多余的神经组织增加，电生理传导改善。相比之下，当DFO诱导的新血管形成被血管内皮生长因子受体抑制剂lenvatinib阻断时，DFO对SCI的改善作用被抑制，这进一步表明DFO在SCI中的主要药理作用是促进新血管形成。因此，我们得出结论，DFO通过促进受损脊髓的新血管形成有效减轻了SCI。考虑到DFO是FDA批准的自由基清除剂和铁螯合剂，因此它可能代表将来有希望的SCI治疗替代策略。我们得出的结论是，DFO通过促进受伤脊髓的新血管形成有效地减轻了SCI。考虑到DFO是FDA批准的自由基清除剂和铁螯合剂，因此它可能代表将来有希望的SCI治疗替代策略。我们的结论是，DFO通过促进受伤脊髓的新血管形成有效地减轻了SCI。考虑到DFO是FDA批准的自由基清除剂和铁螯合剂，因此它可能代表将来有希望的SCI治疗替代策略。