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Background <p>Previous studies have demonstrated that oxidative stress and melanogenesis are regulated by the Wnt/β-catenin signaling pathway. However, the precise mechanism by which the PEDF/Wnt/β-catenin axis modulates apoptosis and melanogenesis remains unclear.</p> Methods <p>Cell viability and mortality rates were assessed using CCK-8 assays and lactate dehydrogenase (LDH) release assays. Mitochondrial ultrastructural changes were analyzed by transmission electron microscopy (TEM). Changes in the mitochondrial membrane potential (ΔΨm) were assessed using the JC-1 fluorescent probe. The effects of PEDF on protein and gene expression were evaluated by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR).</p> Results <p>As the concentration of H<sub>2</sub>O<sub>2</sub> increased, the cell survival rate decreased, which activated the Wnt/β-catenin signaling pathway and increased the apoptosis rate and melanin production. PEDF reversed the H<sub>2</sub>O<sub>2</sub>-induced decrease in cell viability and increase in mortality rate in Melan-a cells while ameliorating the impairment of the mitochondrial membrane potential. PEDF ameliorated H<sub>2</sub>O<sub>2</sub>-induced protein damage and lipid peroxidation and reduced apoptosis in Melan-a cells. PEDF treatment significantly decreased the protein expression levels of β-catenin, Wnt3a, and Dvl2 (<i>P</i> &lt; 0.05) and reduced the protein levels of Bax and Caspase-3 (<i>P</i> &lt; 0.01) in H<sub>2</sub>O<sub>2</sub>- and BML-284-treated Melan-a cells. Furthermore, PEDF significantly reduced the H<sub>2</sub>O<sub>2</sub>- and BML-284-induced increases in the MITF and TYR protein levels (<i>P</i> &lt; 0.01).</p> Conclusions <p>These results suggest that PEDF can reduce H<sub>2</sub>O<sub>2</sub>-induced oxidative damage and melanin production in Melan-a cells by inhibiting the activation of Wnt/β-catenin signaling pathway activation. These findings provide a theoretical basis for human oxidative stress and pigment deposition-related diseases.</p>

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Influence of pigment epithelium-derived factors on H2O2-induced oxidative damage and melanin synthesis in Melan-a cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Yunli Cui,
  • Fuhao Ye,
  • Zengyao Hou,
  • Guohao Li,
  • Luyao Li,
  • Hongxia Zhao,
  • Dongfang Hu,
  • Zhihong Yin,
  • Lingli Chen,
  • Hongmei Ning,
  • Yaming Ge,
  • Quanhai Pang

摘要

Background

Previous studies have demonstrated that oxidative stress and melanogenesis are regulated by the Wnt/β-catenin signaling pathway. However, the precise mechanism by which the PEDF/Wnt/β-catenin axis modulates apoptosis and melanogenesis remains unclear.

Methods

Cell viability and mortality rates were assessed using CCK-8 assays and lactate dehydrogenase (LDH) release assays. Mitochondrial ultrastructural changes were analyzed by transmission electron microscopy (TEM). Changes in the mitochondrial membrane potential (ΔΨm) were assessed using the JC-1 fluorescent probe. The effects of PEDF on protein and gene expression were evaluated by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR).

Results

As the concentration of H2O2 increased, the cell survival rate decreased, which activated the Wnt/β-catenin signaling pathway and increased the apoptosis rate and melanin production. PEDF reversed the H2O2-induced decrease in cell viability and increase in mortality rate in Melan-a cells while ameliorating the impairment of the mitochondrial membrane potential. PEDF ameliorated H2O2-induced protein damage and lipid peroxidation and reduced apoptosis in Melan-a cells. PEDF treatment significantly decreased the protein expression levels of β-catenin, Wnt3a, and Dvl2 (P < 0.05) and reduced the protein levels of Bax and Caspase-3 (P < 0.01) in H2O2- and BML-284-treated Melan-a cells. Furthermore, PEDF significantly reduced the H2O2- and BML-284-induced increases in the MITF and TYR protein levels (P < 0.01).

Conclusions

These results suggest that PEDF can reduce H2O2-induced oxidative damage and melanin production in Melan-a cells by inhibiting the activation of Wnt/β-catenin signaling pathway activation. These findings provide a theoretical basis for human oxidative stress and pigment deposition-related diseases.