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Abstract <p>Diabetic peripheral neuropathy (DPN) is the most common chronic complication in diabetes and considered as the major inducement of lower limb amputation and disabling neuropathic pain in diabetes patients. However, there are currently bottlenecks in DPN treatment. Novel targets and drugs are urgently required for the treatment of DPN. Sappan Wood extract (SWE) could alleviate DPN, yet the mechanism of SWE attenuating DPN remains unclear. Here, SWE was constructed by ethyl acetate, molecular docking study is performed between active ingredients of SWE and target proteins, and Co-immunoprecipitation (Co-IP) was utilized to detect protein phosphorylation. Results indicate that SWE represses cuproptosis of peripheral Schwann cells by brazilin under high glucose (HG) conditions. Mechanism investigation reveals that SWE suppresses cuproptosis by activating AKT serine/threonine kinase 1 (AKT1) via brazilin. Moreover, SWE hinders cuproptosis through inducing ferredoxin 1 (FDX1) phosphorylation by AKT1 via brazilin. Furthermore, AKT1 phosphorylation facilitates FDX1 phosphorylation. In summary, our findings demonstrate that SWE represses cuproptosis of Schwann cells by AKT1-mediated FDX1 phosphorylation via brazilin under HG conditions, which provide novel targets and strategies for DPN treatment.</p>

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Sappan Wood Extract Represses High Glucose-Induced Cuproptosis of Schwann Cells by AKT1-Mediated FDX1 Phosphorylation via Brazilin

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Y. Wang,
  • X. Wang,
  • N. Ren,
  • C. Liu,
  • Y. Shuang,
  • J. Qiu,
  • Y. Liu

摘要

Abstract

Diabetic peripheral neuropathy (DPN) is the most common chronic complication in diabetes and considered as the major inducement of lower limb amputation and disabling neuropathic pain in diabetes patients. However, there are currently bottlenecks in DPN treatment. Novel targets and drugs are urgently required for the treatment of DPN. Sappan Wood extract (SWE) could alleviate DPN, yet the mechanism of SWE attenuating DPN remains unclear. Here, SWE was constructed by ethyl acetate, molecular docking study is performed between active ingredients of SWE and target proteins, and Co-immunoprecipitation (Co-IP) was utilized to detect protein phosphorylation. Results indicate that SWE represses cuproptosis of peripheral Schwann cells by brazilin under high glucose (HG) conditions. Mechanism investigation reveals that SWE suppresses cuproptosis by activating AKT serine/threonine kinase 1 (AKT1) via brazilin. Moreover, SWE hinders cuproptosis through inducing ferredoxin 1 (FDX1) phosphorylation by AKT1 via brazilin. Furthermore, AKT1 phosphorylation facilitates FDX1 phosphorylation. In summary, our findings demonstrate that SWE represses cuproptosis of Schwann cells by AKT1-mediated FDX1 phosphorylation via brazilin under HG conditions, which provide novel targets and strategies for DPN treatment.