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Updated: Mar 31, 2026
Protocol to Create Chronic Wounds in Diabetic Mice
Published on: September 25, 2019
Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in
Yifan Ping1, Jiaying Wang2,1, Shaoyin Wei3
1Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, China.
Abstract:
Hyperglycemia-induced oxidative stress considerably hinders healing of diabetic wounds, primarily due to mitochondrial dysfunction. This pathology leads to an excessive production of reactive oxygen species (ROS), disrupts respiratory chain function, and impairs energy metabolism. This study introduces procyanidin (PC) capsules designed to target the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. The PC capsules demonstrate a sustained ability to scavenge radicals, thereby directly lowering ROS levels and specifically activating the PI3K/AKT pathway. Through this activation, the capsules restore mitochondrial function by reducing mitochondrial reactive oxygen species, stabilizing mitochondrial membrane potential, and restoring energy production. Additionally, cell experiments reveal that the capsules significantly boost the migration of fibroblasts and enhance the angiogenic activity of endothelial cells, indicating the protective effects of PC on crucial cell functions involved in wound healing. In a chronic skin wound model of diabetic mice, the PC capsules are found to accelerate wound closure by promoting collagen deposition, suppressing excessive inflammation, and minimizing mitochondrial oxidative damage. Using the PI3K inhibitor LY294002, we further verified that the pro-migratory and pro-angiogenic effects of PC capsules are largely dependent on the PI3K/AKT signaling pathway. Our novel findings suggest that PC capsules stimulate PI3K/AKT-mediated repair of mitochondrial function, presenting a potential therapeutic approach for treating refractory diabetic wounds.
Insights
Procyanidin (PC) capsules improve diabetic wound healing by reducing oxidative stress and activating the PI3K/AKT pathway. This enhances mitochondrial function and promotes cell repair for faster wound closure.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Wound Healing Research
Background:
- Hyperglycemia in diabetes causes oxidative stress and mitochondrial dysfunction, impairing wound healing.
- Excessive reactive oxygen species (ROS) disrupt cellular energy metabolism and respiratory chain function.
Purpose of the Study:
- To investigate the efficacy of procyanidin (PC) capsules in treating diabetic wounds.
- To elucidate the mechanism of PC action, focusing on the PI3K/AKT pathway and mitochondrial function.
Main Methods:
- Developed procyanidin (PC) capsules targeting the PI3K/AKT pathway.
- Assessed ROS scavenging, mitochondrial function, and cell migration/angiogenesis in vitro.
- Evaluated wound closure, collagen deposition, inflammation, and mitochondrial damage in a diabetic mouse model.
- Utilized PI3K inhibitor LY294002 to confirm pathway dependency.
Main Results:
- PC capsules effectively scavenge ROS, activate the PI3K/AKT pathway, and restore mitochondrial function.
- PC capsules enhanced fibroblast migration and endothelial cell angiogenesis in vitro.
- In vivo, PC capsules accelerated wound closure, increased collagen deposition, and reduced inflammation and mitochondrial damage.
- The pro-migratory and pro-angiogenic effects were confirmed to be PI3K/AKT dependent.
Conclusions:
- PC capsules offer a therapeutic strategy for diabetic wound healing by restoring mitochondrial function via PI3K/AKT activation.
- PC capsules mitigate oxidative stress and inflammation, promoting cellular repair mechanisms essential for wound closure.
