Efeito da própolis verde nos componentes angiogênico, inflamatório e fibrogênico em modelo murino de aderência intraperitoneal

• Ano de defesa: 2012
• Autor(a) principal: Luiza Dias da Cunha Lima
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Extrato aquoso da própolis; Fibrose; Citocinas; Ativação de macrófagos; Própole/uso terapêutico; Complicações pós-operatórias; Experimentação animal; Aderências teciduais; Camundongos
• Link de acesso: http://hdl.handle.net/1843/BUBD-9EGMAL

Intraperitoneal adhesion formation is the major cause of postoperative complications, such as chronic pain, ischemia, bowel obstruction, and infertility. Propolis, a wax bee product has been shown to exhibit multiple actions on tissue repair. Using a model of implant-induced intraperitoneal adhesion in Swiss mice, we showed that systemic treatment with propolis (500/mg/kg/day) was able to decrease intraperitoneal diffusion rate of sodium fluorescein an effect decreasing vascular permeability. In addition, propolis was shown to down regulate angiogenesis (as determined by hemoglobin content) and fibrosis by decreasing the levels of TGF-1 and collagen deposition in the adhesion induced by the synthetic implants. Conversely, the treatment up-regulated inflammatory enzyme activities (myeloperoxidase and n-acethyl--D-glucosaminidase) and TNF- levels. Most importantly, propolis treatment was able to activate both the classical and alternative macrophage pathways, although it was more expressive in M1 macrophages. Approximately 23 fold increase in iNOS and 7 fold increase in IFN- was observed. Increase in gene expression of FIZZ1 and YM1 in the adhesion tissue was also detected after propolis treatment. These observations show for the first time the effects of propolis attenuating adhesion in mice and disclose important mechanisms of actions of the compound (down regulation of angiogenic components and activation of murine macrophage pathways).