Background: The adverse effects of smoking on wound healing of the skin are known clinically. Recently, an endogenous cholinergic pathway for angiogenesis mediated by endothelial nicotinic acetylcholine receptors was discovered. The objective of this study was to investigate the appropriate concentration of nicotine at which angiogenesis and wound healing are accelerated in a murine excisional wound model.
Materials and methods: Full-thickness skin defects (8 mm) were created on the dorsum of C57BL mice and a silicone sheet (8 mm) was sutured. PBS (10 microL), bFGF (1 microg), nicotine (10(-1) M, 10(-3) M, 10(-4) M, 10(-7) M, and 10(-10)M), and both bFGF and 10(-4) M nicotine were topically injected for 7 days. Mice were sacrificed on day 8, and the wound area, the neoepithelium length, and the area of newly formed capillaries were assessed.
Results: The wound area was significantly decreased in the wound treated with bFGF, with 10(-4) M nicotine, and with both bFGF and 10(-4) M nicotine. The length of the epithelium was significantly longer and the area of capillaries was also increased significantly in these three groups. The wound area, the length of the epithelium, and the area of capillaries in the group treated with both bFGF and 10(-4) M nicotine were significantly different from those in the 10(-4) M nicotine-treated group.
Conclusions: In this study, nicotine at a low concentration accelerated angiogenesis and promoted wound healing; these effects of nicotine were synergistic with bFGF.