Effects of Agastache foeniculum essential oil on skin wound healing in mice

Chronic wounds are frequently hindered by high levels of reactive oxygen species, which perpetuate inflammation and delay healing. Antioxidants could mitigate oxidative stress and promote wound repair. This study investigates effectiveness of Agastache foeniculum essential oil in promoting skin wound healing. Thirty-six mice were divided into three groups: Sham (SH), Soybean oil (SB), and Agastache foeniculum (AGS), with each group split into excisional and incisional wounds. Treatments were applied topically for nine days. Wound contraction was measured on days 0, 3, 6, 9, 12, and 14 using ImageJ software. On day 10, biomechanical properties were assessed. Biochemical parameters, including Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), Malondialdehyde (MDA), and Glutathione Peroxidase (GPx), were evaluated on days 7 and 14. Additionally, hydroxyproline levels, Western blot analyses for TNF-α and NF-κB, and histopathological examinations were conducted. The AGS group showed a significant reduction in wound area on days 3, 9, 12, and 14. Increased strain (85.97 %), ultimate strength (9.52 N), and energy storage (13.14 J) was observed in the AGS group compared to controls. MDA levels were significantly lower (0.39, 0.36 nmol/mg protein), and TAC was significantly higher (1.68, 1.8 nmol/mg protein) in the AGS group on both days 7 and 14. Hydroxyproline levels were elevated (90.55 mg/g), and TNF-α was reduced in the AGS group, while NF-κB levels showed a non-significant decrease. Histopathological analysis indicated reduced inflammation and enhanced tissue remodeling in AGS-treated wounds. These findings suggest that Agastache foeniculum essential oil effectively promotes skin wound healing by enhancing contraction, strengthening biomechanical properties, reducing oxidative stress, and modulating inflammation, highlighting its potential as a therapeutic agent in wound management. Also one limitation of this study is the lack of gene expression of the markers.