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<p>This study developed a novel antioxidant fusion protein Prx-LCA2 by conjugating peroxidase Prx with the LCA2 carrier derived from <i>Escherichia coli</i> heat-labile enterotoxin, aiming to achieve efficient intracellular delivery for oxidative damage remediation. The fusion protein Prx-LCA2 was successfully expressed in <i>E. coli</i> and purified. Fluorescence labeling demonstrated efficient cellular internalization of the fusion protein. In vitro, H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in A431 cells was alleviated by Prx-LCA2 treatment, as evidenced by increased cell viability, reduced ROS levels, enhanced antioxidant enzyme activities, and decreased levels of MDA and PCG. In vivo, H<sub>2</sub>O<sub>2</sub>-induced skin oxidative damage in mice was significantly ameliorated by Prx-LCA2 treatment, including improvement in antioxidant enzyme activities and reduction in oxidative damage markers (MDA, PCG and 8-OHdG). Additionally, Prx-LCA2 increased HYP content in the skin, indicating improved collagen integrity. Histological analysis of mouse skin further confirmed the therapeutic efficacy of Prx-LCA2. The enterotoxin-derived carrier system exhibited excellent biosafety profile with no observed cytotoxicity or skin irritation. This microbial-based protein engineering strategy provides a promising platform for transdermal delivery of antioxidant therapeutics.</p>

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Engineered Prx-LCA2 fusion protein restores oxidative skin damage via enhanced intracellular peroxidase delivery

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月18日

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  • Di Liu,
  • Yafen Zhan,
  • Jiaqi Qu,
  • Hongping Qiao,
  • Na Li,
  • Yeli Zhang,
  • Xiaoying Wu

摘要

This study developed a novel antioxidant fusion protein Prx-LCA2 by conjugating peroxidase Prx with the LCA2 carrier derived from Escherichia coli heat-labile enterotoxin, aiming to achieve efficient intracellular delivery for oxidative damage remediation. The fusion protein Prx-LCA2 was successfully expressed in E. coli and purified. Fluorescence labeling demonstrated efficient cellular internalization of the fusion protein. In vitro, H2O2-induced oxidative stress in A431 cells was alleviated by Prx-LCA2 treatment, as evidenced by increased cell viability, reduced ROS levels, enhanced antioxidant enzyme activities, and decreased levels of MDA and PCG. In vivo, H2O2-induced skin oxidative damage in mice was significantly ameliorated by Prx-LCA2 treatment, including improvement in antioxidant enzyme activities and reduction in oxidative damage markers (MDA, PCG and 8-OHdG). Additionally, Prx-LCA2 increased HYP content in the skin, indicating improved collagen integrity. Histological analysis of mouse skin further confirmed the therapeutic efficacy of Prx-LCA2. The enterotoxin-derived carrier system exhibited excellent biosafety profile with no observed cytotoxicity or skin irritation. This microbial-based protein engineering strategy provides a promising platform for transdermal delivery of antioxidant therapeutics.