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<p>Boric acid (BA), a boron-based compound with known antimicrobial and anti-inflammatory properties, has recently attracted attention for its potential role in enhancing wound healing. However, its effects on keratinocyte-mediated skin repair at the molecular level remain underexplored. This study aimed to evaluate the impact of BA on wound healing using HaCaT keratinocytes. Cell viability was assessed following 24 and 48&#xa0;h exposure to increasing concentrations of BA (0-2500 µM). Non-cytotoxic concentrations (10, 100 and 250 µM) were selected for subsequent analyses. Scratch assays were performed to evaluate cell migration. qRT-PCR was used to evaluate the expression levels of key genes associated with cell adhesion, proliferation, and epithelial-mesenchymal transition (CTNNA1, CTNNB1, ILK, OCLN, VIM, MMP7, MMP9, ZEB1 and ZEB2). BA treatment significantly enhanced wound closure in a dose-dependent manner, with the 250 µM group showing the highest closure rate (~ 50%) at 48&#xa0;h. BA upregulated CTNNA1, CTNNB1, ILK, VIM, OCLN, MMP7 and ZEB2 expression levels. In contrast, ZEB1 expression was slightly decreased, while MMP9 level remained unchanged. At the protein level, VIM and ZEB2 were both upregulated. These findings suggest that BA promotes wound healing in keratinocytes by enhancing cell migration and modulating the expression of key genes involved in tissue regeneration. BA may represent a promising candidate for topical wound healing therapies.</p>

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Boric Acid Stimulates Wound Closure and Modulates EMT-Related Gene Expression in HaCaT Cells

  • 期刊论文

  • 发表日期：

    2025年12月22日

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  • Sedef Akçaalan,
  • Canan Eroğlu Güneş,
  • Ercan Kurar

摘要

Boric acid (BA), a boron-based compound with known antimicrobial and anti-inflammatory properties, has recently attracted attention for its potential role in enhancing wound healing. However, its effects on keratinocyte-mediated skin repair at the molecular level remain underexplored. This study aimed to evaluate the impact of BA on wound healing using HaCaT keratinocytes. Cell viability was assessed following 24 and 48 h exposure to increasing concentrations of BA (0-2500 µM). Non-cytotoxic concentrations (10, 100 and 250 µM) were selected for subsequent analyses. Scratch assays were performed to evaluate cell migration. qRT-PCR was used to evaluate the expression levels of key genes associated with cell adhesion, proliferation, and epithelial-mesenchymal transition (CTNNA1, CTNNB1, ILK, OCLN, VIM, MMP7, MMP9, ZEB1 and ZEB2). BA treatment significantly enhanced wound closure in a dose-dependent manner, with the 250 µM group showing the highest closure rate (~ 50%) at 48 h. BA upregulated CTNNA1, CTNNB1, ILK, VIM, OCLN, MMP7 and ZEB2 expression levels. In contrast, ZEB1 expression was slightly decreased, while MMP9 level remained unchanged. At the protein level, VIM and ZEB2 were both upregulated. These findings suggest that BA promotes wound healing in keratinocytes by enhancing cell migration and modulating the expression of key genes involved in tissue regeneration. BA may represent a promising candidate for topical wound healing therapies.