Effect and mechanism of frankincense on wound healing of full-thickness skin defects in diabetic rats

HAN Zi-yang; WU Wei-ping; BAI Ze-ming; HUANG Hai; GUAN Hong-jian; ZHOU Da-peng

doi:10.16048/j.issn.2095-5561.2025.02.10

Abstract：Objective To investigate the promotive effect of frankincense on wound healing in full-thickness skin defects in diabetic rats and explore its underlying mechanisms.Methods Thirty male Sprague-Dawley(SD)rats were randomly divided into three groups(n=10 each):control group,normal saline group,and frankincense group.Diabetic models were established in the normal saline and frankincense groups.A 2 cm diameter full-thickness skin defect wound was created on the dorsal midline of all rats.The frankincense group received daily oral administration of 1 g frankincense granule solution,while the normal saline and control groups were administered an equivalent volume of normal saline.Wound healing was assessed every 3 days postoperatively.The number of positive cells per visual field of platelet endothelial cell adhesion molecule-1(CD31)and tumor necrosis factor-α(TNF-α)were evaluated by immunohistochemical staining.Total protein was extracted from wound margin tissues to measure vascular endothelial growth factor(VEGF)and TNF-α expression levels.Results The wound healing speed of frankincense group was higher than that of normal saline group,the average collagen density of wound was higher than that of normal saline group,the number of CD31 cells per field of wound tissue was higher than that of normal saline group,the number of TNF-α positive cells per field of wound tissue was lower than that of normal saline group,the relative expression of VEGF in wound tissue was higher than that of normal saline group,and the relative expression of TNF-αwas lower than that of normal saline group.The differences were statistically significant(P＜0.05).Conclusion Frankincense facilitates wound healing in diabetic rats with full-thickness skin defects through mechanisms involving inflammation modulation and angiogenesis promotion.