Gas Plasma Exposure Alters Microcirculation and Inflammation during Wound Healing in a Diabetic Mouse Model.
Anke SchmidtDebora SingerHenrike AdenThomas von WoedtkeSander BekeschusPublished in: Antioxidants (Basel, Switzerland) (2024)
Diabetes can disrupt physiological wound healing, caused by decreased levels or impaired activity of angiogenic factors. This can contribute to chronic inflammation, poor formation of new blood vessels, and delayed re-epithelialization. The present study describes the preclinical application of medical gas plasma to treat a dermal, full-thickness ear wound in streptozotocin (STZ)-induced diabetic mice. Gas plasma-mediated effects occurred in both sexes but with gender-specific differences. Hyperspectral imaging demonstrated gas plasma therapy changing microcirculatory parameters, particularly oxygen saturation levels during wound healing, presumably due to the gas plasma's tissue delivery of reactive species and other bioactive components. In addition, gas plasma treatment significantly affected cell adhesion by regulating focal adhesion kinase and vinculin, which is important in maintaining skin barrier function by regulating syndecan expression and increasing re-epithelialization. An anticipated stimulation of blood vessel formation was detected via transcriptional and translational increase of angiogenic factors in gas plasma-exposed wound tissue. Moreover, gas plasma treatment significantly affected inflammation by modulating systemic growth factors and cytokine levels. The presented findings may help explain the mode of action of successful clinical plasma therapy of wounds of diabetic patients.
Keyphrases
- skeletal muscle
- wound healing
- insulin resistance
- room temperature
- mouse model
- oxidative stress
- type diabetes
- metabolic syndrome
- escherichia coli
- high resolution
- carbon dioxide
- cell adhesion
- signaling pathway
- cardiovascular disease
- mental health
- mesenchymal stem cells
- weight loss
- replacement therapy
- protein kinase
- optical coherence tomography
- drug induced
- endothelial cells