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  11. Orthosilicic Acid Promotes Diabetic Wound Healing Through The Pi3 K/akt/mtor Signaling Pathway

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

Xinhui Wu1,2, Jincheng Liu3, Wenting Song1,4

  • 1Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, 250001, People's Republic of China.

Biological Trace Element Research
|June 14, 2025

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View abstract on PubMed

Summary
This summary is machine-generated.

Orthosilicic acid (OSA) promotes human umbilical vein endothelial cell (HUVEC) proliferation, migration, and angiogenesis in high-glucose conditions. OSA also inhibits HUVEC apoptosis, offering a potential therapeutic strategy for diabetic wound healing.

Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Wound Healing Research

Background:

  • Diabetic wound healing is significantly impaired due to high-glucose-induced endothelial cell dysfunction.
  • Orthosilicic acid (OSA), a bioavailable silicon form, has not been studied for its effects on diabetic wound healing.
  • Endothelial cell impairment is a key factor in delayed healing of diabetic wounds.

Purpose of the Study:

  • To investigate the potential of Orthosilicic acid (OSA) in promoting diabetic wound healing.
  • To determine the effects of OSA on human umbilical vein endothelial cells (HUVECs) under high-glucose conditions.
  • To elucidate the molecular pathways involved in OSA's therapeutic effects on diabetic wounds.

Main Methods:

  • CCK-8, EdU, Transwell, and cell-scratch assays were used to assess HUVEC proliferation and migration.
Keywords:
DiabetesHUVECsMMSTOSA

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  • Tube-formation assays evaluated the impact of OSA on angiogenesis.
  • TUNEL and flow cytometry were employed to analyze HUVEC apoptosis.
  • In vivo studies utilized db/db mice to assess wound healing efficacy and the PI3K/AKT/mTOR pathway.

    • Main Results:

    • OSA at 30 μM optimally promoted HUVEC proliferation and migration in high-glucose environments.
    • OSA treatment rescued high-glucose-induced inhibition of HUVEC angiogenesis.
    • OSA significantly inhibited high-glucose-induced HUVEC apoptosis.
    • In vivo, OSA accelerated skin wound healing in db/db mice via the PI3K/AKT/mTOR pathway.

    Conclusions:

    • Orthosilicic acid (OSA) demonstrates significant potential in promoting diabetic wound healing by enhancing endothelial cell function.
    • OSA promotes HUVEC proliferation, migration, angiogenesis, and inhibits apoptosis under hyperglycemic conditions.
    • The PI3K/AKT/mTOR pathway is implicated in OSA's beneficial effects on diabetic wound healing, suggesting OSA as a promising therapeutic agent.
    PI3 K
    Wounds