Β2 agonist (Salbutamol) modulate skin wound healing processes

Abstract

Wound healing is a complex physiological and dynamic process required the coordination of numerous cell types and biological processes to regenerate damaged tissue and initiate repair which is dependent on a number of inter-related factors. This study was aimed to demonstrate whether the β2 receptor has role in wound healing and angiogenesis. A murine wild-type (in vivo), excisional skin wound model was done to demonstrate that activation of β2AR delay wound repair, twenty-four male albino mice were used to investigate the effect of the drug on experimental wound healing grossly, histopathologically and immune-histochemically compared with vehicle-only controls. The results showed that the rate of wound healing was significantly slower in salbutamol group than in control group (P<0.05) after being followed for 5 days for some of the animals and for 10 days for other animals from the third day and thereafter. The results also revealed that in 10 days the mean immunohistochemical scores were significantly higher than that in 5 days for all groups and for all markers enrolled in the present study (P<0.05). Adding salbutamol significantly reduced collagen III, SMA and CD31 mean immunohistochemical score in days 5 and 10 when compared to control group (P<0.05). The current study concluded that the administration of β2 adrenergic receptor agonist (salbutamol) delays wound healing through reduction of angiogenesis, collagen III deposition, myofibroblast density and re-epithelialization process.