Metformin lotion promotes scarless skin tissue formation through AMPK activation, TGF-β1 inhibition, and reduced myofibroblast numbers

PLoS One. 2024 Sep 27;19(9):e0311147. doi: 10.1371/journal.pone.0311147. eCollection 2024.

Abstract

Scar tissue formation following skin wound healing is a challenging public health problem. Skin regeneration and preventing the formation of scar tissue by currently available commercial products are largely ineffective. This study aimed to test the efficacy of a novel topical metformin lotion (ML) in inhibiting scar tissue formation during skin wound healing in rats and to determine the mechanisms of action involved. A 6% ML was prepared in our laboratory. A skin wound healing model in rats was used. The wounded rats were divided into two groups and treated daily for 10 days as follows: Group 1 received a daily application of 50 mg of control lotion, or 0% ML (totaling 100 mg of lotion per rat), and Group 2 received a daily application of 50 mg of 6% ML (totaling 100 mg of 6% ML per rat). Blood samples from the heart of each rat were analyzed for inflammatory markers, HMGB1 and IL-1β, using ELISA, and immunological and histological analyses were performed on skin tissue sections. ML decreased levels of inflammatory markers HMGB1 and IL-1β in the serum of rats and inhibited the release of HMGB1 from cell nuclei into the skin tissue matrix. Additionally, ML demonstrated anti-fibrotic properties by enhancing AMPK activity, decreasing the expression of TGF-β1, reducing the number of myofibroblasts, decreasing the production of collagen III, and increasing the expression of collagen I. ML promotes the regeneration of high-quality skin during wound healing by reducing scar tissue formation. This effect is mediated through the activation of AMPK, inhibition of TGF-β1, and a decrease in the number of myofibroblasts.

MeSH terms

  • AMP-Activated Protein Kinases* / metabolism
  • Animals
  • Cicatrix* / drug therapy
  • Cicatrix* / metabolism
  • Cicatrix* / pathology
  • Cicatrix* / prevention & control
  • HMGB1 Protein / metabolism
  • Interleukin-1beta / metabolism
  • Male
  • Metformin* / pharmacology
  • Myofibroblasts* / drug effects
  • Myofibroblasts* / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Skin* / drug effects
  • Skin* / metabolism
  • Skin* / pathology
  • Transforming Growth Factor beta1* / metabolism
  • Wound Healing* / drug effects

Substances

  • Metformin
  • Transforming Growth Factor beta1
  • AMP-Activated Protein Kinases
  • Interleukin-1beta
  • HMGB1 Protein
  • Hbp1 protein, rat

Grants and funding

This work was supported in part by a DOD/MTEC Award (W81XWH2290016) https://mtec-sc.org/ to JW and Pittsburgh Foundation Albert B. Ferguson, Jr. MD. Orthopaedic Fund Awards (AD2021-120112; AD2022-130408; AD2023-134256) to JZ. The funders did not play any role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.