Protective effect of botulinum toxin A after cutaneous XXXX -reperfusion injury.

@entity4094 @entity63 @entity19 @entity1066 @entity26 @entity1119 @entity519 @entity5231 @entity6227 @entity934
UNASSIGNED: Botulinum toxin A (BTX-A) blocks the release of @entity934 vesicles into the synaptic space, and has been clinically used for aesthetic indications, @entity4094 and @entity1119 . Several studies have demonstrated that BTX-A enhanced the blood flow and improved @entity63 in animal models. Our objective was to assess the effects of BTX-A on cutaneous @entity63 -reperfusion (I/R) injuries, mimicking @entity6227 . The administration of BTX-A in I/R areas significantly inhibited the formation of @entity6227 -like @entity1066 in cutaneous I/R injury @entity19 model. The number of @entity5231 (+) vessels and aSMA(+) pericytes or myofibroblasts in wounds were significantly increased in the I/R @entity19 treated with BTX-A. The @entity519 area and the number of oxidative stress-associated DNA-damaged cells and apoptotic cells in the I/R sites were reduced by BTX-A administration. In an in vitro assay, BTX-A significantly prevented the oxidant-induced intracellular accumulation of reactive @entity26 species (ROS) in vascular endothelial cells. Furthermore, the administration of BTX-A completely suppressed the @entity1066 formation in an intermittent short-time cutaneous I/R injury model. These results suggest that BTX-A might have protective effects against @entity1066 formation after cutaneous I/R injury by enhancing angiogenesis and inhibiting @entity519 -induced cellular damage. Exogenous application of BTX-A might have therapeutic potential for cutaneous I/R injuries.
