Effect of Atorvastatin on Wound Healing in Rats

Autor(es)

Suzuki-Banhesse, Vanessa Ferraz ^[1] ; Azevedo, Flavia Figueiredo ^[1] ; Araujo, Eliana Pereira ^[1] ; Corezola do Amaral, Maria Esmeria ^[2] ; Caricilli, Andrea Moro ^[3] ; Abdalla Saad, Mario Jose ^[4] ; Melo Lima, Maria Helena ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Campinas, Fac Nursing, BR-13081970 Campinas, SP - Brazil

^[2] UNIARARAS, Herminio Ometto Univ Ctr, Araras, SP - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo - Brazil

^[4] Univ Estadual Campinas, Fac Med Sci, Dept Internal Med, BR-13081970 Campinas, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Biological Research for Nursing; v. 17, n. 2, p. 159-168, MAR 2015.
• Citações Web of Science: 7

Resumo

Skin-wound healing is a complex and dynamic biological process involving inflammation, proliferation, and remodeling. Recent studies have shown that statins are new therapeutical options because of their actions, such as anti-inflammatory and antioxidant activity, on vasodilation, endothelial dysfunction and neoangiogenesis, which are independent of their lipid-lowering action. Our aim was to investigate the effect of atorvastatin on tissue repair after acute injury in healthy animals. Rats were divided into four groups: placebo-treated (P), topical atorvastatin-treated (AT), oral atorvastatin-treated (AO), topical and oral atorvastatin-treated (ATO). Under anesthesia, rats were wounded with an 8-mm punch in the dorsal region. Lesions were photographed on Days 0, 1, 3, 7, 10, 12, and 14 post-injury and samples taken on Days 1, 3, 7, and 14 for protein-expression analysis of insulin receptor substrate (IRS)-1, phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), glycogen synthase kinase (GSK)-3, endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), extracellular signal-regulated kinase (ERK), interleukin (IL)-10, IL-1, IL-6, and tumor necrosis factor (TNF)-. Upon macroscopic examination, we observed significant reductions of lesion areas in groups AT, AO, and ATO compared to the P group. Additionally, AT and AO groups showed increased expression of IRS-1, PI3K, Akt, GSK-3, and IL-10 on Days 1 and 3 when compared with the P group. All atorvastatin-treated groups showed higher expression of IRS-1, PI3K, Akt, GSK-3, IL-10, eNOS, VEGF, and ERK on Day 7. On Days 1, 3, and 7, all atorvastatin-treated groups showed lower expression of IL-6 and TNF- when compared with the P group. We conclude that atorvastatin accelerated tissue repair of acute lesions in rats and modulated expressions of proteins and cytokines associated with cell-growth pathways. (AU)

• Processo FAPESP: 12/14406-6 - Cicatrização e sinalização de insulina: fenofibrato, estatinas e queimaduras.
• Beneficiário: Maria Helena de Melo Lima
• Modalidade de apoio: Auxílio à Pesquisa - Regular