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<p>Delayed healing of diabetic wounds is one of the major complications of diabetes mellitus, which increases the rate of amputation and mortality in patients. The impairment of vascular endothelial cells in a high-glucose environment is one of the main reasons for the delayed healing of diabetic wounds. Orthosilicic acid (OSA), the primary bioavailable form of silicon, has not yet been investigated for its potential role in the delayed healing of diabetic wounds. The CCK-8 experiment confirmed that 30&#xa0;μM was the optimal concentration for OSA to affect the proliferation of human umbilical vein endothelial cells (HUVECs). EdU, Transwell, and cell-scratch experiments verified that OSA promoted the proliferation and migration ability of HUVECs under a high-glucose environment. The result of the tube-formation experiment demonstrated that OSA rescued the inhibition of HUVECs angiogenesis caused by a high-glucose environment. TUNEL and flow cytometry revealed that OSA inhibited the apoptosis of HUVECs induced by a high-glucose environment. In vivo experiments revealed that OSA could promote the healing of skin wounds in db/db mice through the PI3K/AKT/mTOR pathway. Our findings suggested that OSA promoted angiogenesis in HUVECs via the PI3K-AKT/mTOR pathway and emphasized that OSA is a potential therapeutic strategy for treating diabetic wounds.</p>

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Orthosilicic Acid Promotes Diabetic Wound Healing Through the PI3 K/AKT/mTOR Signaling Pathway

  • 期刊论文

  • 发表日期：

    2025年6月14日

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  • Xinhui Wu,
  • Jincheng Liu,
  • Wenting Song,
  • Lanxia Wu,
  • Qingyang Fu,
  • Junfei Chen,
  • Qiu Li

摘要

Delayed healing of diabetic wounds is one of the major complications of diabetes mellitus, which increases the rate of amputation and mortality in patients. The impairment of vascular endothelial cells in a high-glucose environment is one of the main reasons for the delayed healing of diabetic wounds. Orthosilicic acid (OSA), the primary bioavailable form of silicon, has not yet been investigated for its potential role in the delayed healing of diabetic wounds. The CCK-8 experiment confirmed that 30 μM was the optimal concentration for OSA to affect the proliferation of human umbilical vein endothelial cells (HUVECs). EdU, Transwell, and cell-scratch experiments verified that OSA promoted the proliferation and migration ability of HUVECs under a high-glucose environment. The result of the tube-formation experiment demonstrated that OSA rescued the inhibition of HUVECs angiogenesis caused by a high-glucose environment. TUNEL and flow cytometry revealed that OSA inhibited the apoptosis of HUVECs induced by a high-glucose environment. In vivo experiments revealed that OSA could promote the healing of skin wounds in db/db mice through the PI3K/AKT/mTOR pathway. Our findings suggested that OSA promoted angiogenesis in HUVECs via the PI3K-AKT/mTOR pathway and emphasized that OSA is a potential therapeutic strategy for treating diabetic wounds.