4.5 Article

Olive oil promotes wound healing of mice pressure injuries through NOS-2 and Nrf2

期刊

APPLIED PHYSIOLOGY NUTRITION AND METABOLISM
卷 44, 期 11, 页码 1199-1208

出版社

CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/apnm-2018-0845

关键词

olive oil; pressure lesion; skin; mouse; wound healing; diet

资金

  1. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
  2. Fundacao de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ)
  3. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  4. CAPES

向作者/读者索取更多资源

The pressure injury environment is characterized by overproduction of reactive oxygen species and exacerbated inflammation, which impair the healing of these lesions. Mediterranean-like diet may be a good intervention to improve the healing of pressure injury owing to its anti-inflammatory and antioxidant components. Thus, this study evaluated the hypothesis that olive oil, as a main source of lipid in Mediterranean diet, could improve cutaneous wound healing of pressure injury in mice. Male Swiss mice were randomly divided into standard, olive oil, or soybean oil plus olive oil groups and fat represented 10% of total calories in all groups. Four weeks after the beginning of diet administration, 2 cycles of ischemia-reperfusion (IR) by external application of 2 magnets disks were performed in the dorsal skin to induce pressure injury formation. Fourteen days after the end of the second IR cycle, olive oil-based diet reduced neutrophils cells and cyclooxygenase-2 protein expression and increased nitric oxide synthase-2 and protein and lipid oxidation. Olive oil based-diet also increased nuclear factor erythroid 2-related factor 2 protein expression and collagen type I precursor protein expression. In addition, administration of olive oil-based diet promoted wound closure at 7, 10, and 14 days after the end of the second IR cycle. These findings support the hypothesis that olive oil-based diet improves cutaneous wound healing of pressure injury in mice through the reduction of inflammation and stimulation of redox equilibrium.

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