Ácido cafeico fenetil éster antecipa as fases do reparo de úlceras de pressão em camundongo

• Autor(a) principal: Bandeira, Luana Graziella
• Data de Publicação: 2017
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UERJ
• Texto Completo: http://www.bdtd.uerj.br/handle/1/12800
• topic: Cutaneous wound healing; Pressure ulcer; Ischemia and reperfusion; Caffeic acid phenethyl ester; Reparo tecidual cutâneo; Úlcera de pressão; Isquemia e reperfusão; Ácido cafeico fenetil éster; Úlcera por pressão; Pele Reparos e reconstrução; Cicatrização de feridas; Agentes anti-inflamatórios; Lesão por pressão; CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::HISTOLOGIA

Pressure ulcers are lesions created by inflammation and oxidative damage induced by cycles of ischemia and reperfusion (IR). Caffeic acid phenethyl ester (CAPE) is a compound extracted from propolis of bees and modified pharmacologically which has anti-inflammatory and antioxidant potential. Therefore, the aim of this work was to evaluate the effects of CAPE in wound healing of pressure ulcers induced by repeated cycles of IR in mice. For this, male Swiss mice (n = 44) underwent a noninvasive model of pressure ulcer induced by two cycles of IR. After ulcer formation, one group of animals was treated intraperitoneally with 5 μmol / kg of CAPE (n = 22) (CAPE group) and another group received only vehicle solution (n = 22) (control group) daily until the end of the experiment. The ulcers were photographed, measured and collected and processed for histology 3, 7 and 12 days after the last IR cycle (d3, d7, d12), or frozen and lysed for biochemistry in d3, d7 and d12, or lysed in TRIzol reagent for extraction of messenger RNA in d3. The administration of CAPE anticipated the protein expression of NOS-2, COX-2 and TNF-α and the gene expression of TNF-α. CAPE anticipated gene and protein expression and NF-κB activity when compared to the control group. In addition, CAPE anticipated the infiltration of macrophages and neutrophils throughout the experiment in the ulcer area when compared to the control. CAPE increased the protein expression of NRF2 in d12, reduced damage to lipids and the neutrophil pro elastase synthesis on all evaluated days, anticipated the expression of nitrotyrosine, MMP-1 and MMP-12 during the experiment and increased the expression of MMP-8 on all evaluated days in relation to the control group. CAPE reduced VEGF expression in d3 and increased angiogenesis at the beginning of the experiment in relation to the control group. CAPE increased the expression of TGF-β1 in d3, reduced the volume of myofibroblasts in d12, increased the proliferation of keratinocytes in d3 and reduced in d7, and reduced cell proliferation in the dermis in d12 when compared to control. In addition, administration of CAPE accelerated the collagen turnover when compared to the control group. Finally, treatment with CAPE reduced the percentage of original ulcer area on all evaluated days and increased the re-epithelialized area in d12 in relation to the control group. In conclusion, administration of CAPE accelerated the tissue repair of pressure ulcers induced by IR cycles in mice probably for anticipating the stages of tissue repair.