Olive oil-induced reduction of oxidative damage and inflammation promotes wound healing of pressure ulcers in mice.
BACKGROUND
The overproduction of reactive oxygen species (ROS) and exacerbated inflammatory response are the main events that impair healing of pressure ulcers. Therefore, olive oil may be a good alternative to improve the healing of these chronic lesions due to its anti-inflammatory and antioxidant properties.


OBJECTIVE
This study investigated the effect of olive oil administration on wound healing of pressure ulcers in mice.


METHODS
Male Swiss mice were daily treated with olive oil or water until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induced pressure ulcer formation.


RESULTS
The olive oil administration accelerated ROS and nitric oxide (NO) synthesis and reduced oxidative damage in proteins and lipids when compared to water group. The inflammatory cell infiltration, gene tumor necrosis factor-α (TNF-α) expression and protein neutrophil elastase expression were reduced by olive oil administration when compared to water group. The re-epithelialization and blood vessel number were higher in the olive oil group than in the water group. The olive oil administration accelerated protein expression of TNF-α, active transforming growth factor-β1 and vascular endothelial growth factor-A when compared to water group. The collagen deposition, myofibroblastic differentiation and wound contraction were accelerated by olive oil administration when compared to water group.


CONCLUSIONS
Olive oil administration improves cutaneous wound healing of pressure ulcers in mice through the acceleration of the ROS and NO synthesis, which reduces oxidative damage and inflammation and promotes dermal reconstruction and wound closure.
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Aline
A
Donato-Trancoso
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Andréa
A
Monte-Alto-Costa
Department of Histology and Embryology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: bruna.souza@uerj.br.
Bruna
B
Romana-Souza
D000279:Administration, Cutaneous; D000818:Animals; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D008297:Male; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism*; D000069463:Olive Oil / Q000008:administration & dosage / Q000627:therapeutic use*; D003668:Pressure Ulcer / Q000188:drug therapy*; D062326:Re-Epithelialization / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012867:Skin / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects*
D000069463:Olive Oil; D017382:Reactive Oxygen Species; C508961:Tgfb1 protein, mouse; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D009569:Nitric Oxide; D003094:Collagen
Cutaneous wound healing; Inflammation; Mice; Olive oil; Oxidative damage; Pressure ulcer