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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Effect of Atorvastatin on Wound Healing in Rats

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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]
Total Authors: 7
[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
Total Affiliations: 4
Document type: Journal article
Source: Biological Research for Nursing; v. 17, n. 2, p. 159-168, MAR 2015.
Web of Science Citations: 7

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)

Grantee:Maria Helena de Melo Lima
Support type: Regular Research Grants