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Bone Marrow Mesenchymal Stem Cells-derived Exosomes Promote Survival of Random Flaps in Rats through Nrf2-mediated Antioxidative Stress

  • 0Department of Oral and Maxillofacial-Head and Neck Oncology, Beijing Stomatological Hospital, Capital Medical University, Beijing, People's Republic of China.
Journal of Reconstructive Microsurgery +

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May 23, 2024

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May 23, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exo) significantly improve random flap survival by reducing oxidative stress and inflammation. These exosomes activate the Keap1/Nrf2 pathway, offering a novel therapeutic strategy against flap necrosis.

Area Of Science

  • Regenerative Medicine
  • Biomaterials Science
  • Wound Healing Research

Background

  • Random flaps are crucial for head and neck reconstruction but are prone to necrosis due to oxidative stress (OS).
  • Exosomes from stem cells possess regenerative and antioxidant properties.
  • Nuclear factor erythroid-2-related factor 2 (Nrf2) is key in managing OS.

Purpose Of The Study

  • To investigate the antioxidant effects and underlying mechanisms of bone marrow mesenchymal stem cells-derived exosomes (BMSCs-Exo) on random flaps.
  • To evaluate the therapeutic potential of BMSCs-Exo in preventing random flap necrosis.

Main Methods

  • BMSCs-Exo were administered intravenously to rats with random flaps on days 0, 1, and 2 post-surgery.
  • Flap survival rates were assessed on day 3.
  • Oxidative stress markers, apoptosis, inflammation, angiogenesis, and mitochondrial function were evaluated using various assays and staining techniques, including in vitro studies with Nrf2 inhibition.

Main Results

  • BMSCs-Exo significantly enhanced random flap survival rates.
  • Treatment reduced apoptosis, inflammation, and OS, while promoting angiogenesis and increasing mitochondrial membrane potential.
  • Therapeutic effects were linked to the activation of the Kelch-like enyol-CoA hydratase (ECH)-associated protein 1 (Keap1)/Nrf2 signaling pathway.

Conclusions

  • BMSCs-Exo enhance tissue antioxidant capacity by modulating the Keap1/Nrf2 pathway.
  • BMSCs-Exo represent a promising new strategy to combat random flap necrosis.