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<p>Impaired wound healing in diabetic patients is a major clinical challenge, often associated with mitochondrial dysfunction and oxidative stress. Excessive ROS production increases inflammation and disrupts tissue regeneration. Current wound treatments primarily target infection control and wound closure, but do not address the underlying factors. Therefore, there is a critical need for therapies that target the underlying mechanisms sustaining impaired healing in diabetic wounds. This study investigates the therapeutic potential of benfotiamine in promoting diabetic wound healing by modulating Trisk95 expression and reducing oxidative stress. Molecular docking for benfotiamine-Trisk95 interaction and KEGG pathway analysis of benfotiamine-targeted genes were performed, which are related to diabetic complications. In vivo experimentation was conducted in diabetic mouse models, and benfotiamine was applied topically to the wounds to examine its effect on wound healing rate. The expression of Trisk95, IL-6, and IL-10 genes was analyzed, and antioxidant effects were evaluated by analyzing ROS levels. In in silico studies, molecular docking showed stable binding of benfotiamine to Trisk95, indicating a strong ligand–protein interaction. The KEGG analysis showed that benfotiamine-targeted genes are crucial mediators of oxidative stress and inflammation in diabetic complications and are linked to mitochondrial function. In vivo studies confirmed that Trisk95 expression is upregulated in diabetic mice as compared to non-diabetic mice. Further experiments showed that benfotiamine accelerates wound closure by significantly downregulating Trisk95 and IL-6, while upregulating IL-10 expression. Furthermore, benfotiamine increased the activity of antioxidant enzymes, including superoxide dismutase and Catalase, resulting in reduced ROS levels in wound tissues. In conclusion, these findings suggest that benfotiamine may be a potential candidate for promoting mitochondrial function and skin regeneration, which ameliorate wound healing in diabetic mice by modulating Trisk95 and exhibiting anti-inflammatory and antioxidant effects.</p>

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Benfotiamine promotes diabetic wound healing by modulating Trisk95 and reducing oxidative stress

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月7日

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  • Shumail Maqbool,
  • Hussain M. Wahedi

摘要

Impaired wound healing in diabetic patients is a major clinical challenge, often associated with mitochondrial dysfunction and oxidative stress. Excessive ROS production increases inflammation and disrupts tissue regeneration. Current wound treatments primarily target infection control and wound closure, but do not address the underlying factors. Therefore, there is a critical need for therapies that target the underlying mechanisms sustaining impaired healing in diabetic wounds. This study investigates the therapeutic potential of benfotiamine in promoting diabetic wound healing by modulating Trisk95 expression and reducing oxidative stress. Molecular docking for benfotiamine-Trisk95 interaction and KEGG pathway analysis of benfotiamine-targeted genes were performed, which are related to diabetic complications. In vivo experimentation was conducted in diabetic mouse models, and benfotiamine was applied topically to the wounds to examine its effect on wound healing rate. The expression of Trisk95, IL-6, and IL-10 genes was analyzed, and antioxidant effects were evaluated by analyzing ROS levels. In in silico studies, molecular docking showed stable binding of benfotiamine to Trisk95, indicating a strong ligand–protein interaction. The KEGG analysis showed that benfotiamine-targeted genes are crucial mediators of oxidative stress and inflammation in diabetic complications and are linked to mitochondrial function. In vivo studies confirmed that Trisk95 expression is upregulated in diabetic mice as compared to non-diabetic mice. Further experiments showed that benfotiamine accelerates wound closure by significantly downregulating Trisk95 and IL-6, while upregulating IL-10 expression. Furthermore, benfotiamine increased the activity of antioxidant enzymes, including superoxide dismutase and Catalase, resulting in reduced ROS levels in wound tissues. In conclusion, these findings suggest that benfotiamine may be a potential candidate for promoting mitochondrial function and skin regeneration, which ameliorate wound healing in diabetic mice by modulating Trisk95 and exhibiting anti-inflammatory and antioxidant effects.