Avaliação da atividade da Jararagina-C na resposta inflamatória induzida por implantes de esponja em camundongos

Abstract

Inflammation and angiogenesis act simultaneously on various chronic diseases. Many of these processes are mediated by interaction between extracellular matrix and integrin transmembrane receptors. The jararhagin-C (Jar-C) is a disintegrin-like protein, isolated from the venom of the viper Bothrops jararaca. Studies showed its effects on cell adhesion mediated by type I collagen and the capacity to modulate various aspects of cellular activity by association with integrin α2β1. Our objective was to investigate the effects of jararhagin-C on key components of the inflammatory response induced by a model of synthetic implants sponge in mice. The treatment with JAR-C was capable of amplifying the inflammatory response changing at certain doses some major components of fibrovascular tissue induced by subcutaneous synthetic implants also modulating fibrogenesis. The proinflammatory effects were observed by increasing the enzyme activity of neutrophils and macrophages (MPO and NAG, respectively), as well as the increased production of chemokines CXCL-1 / KC and CCL2-JE-MCP 1 involved in the recruitment of these cell types as well as by the increased production of TNF-α cytokine. As for the angiogenic component, were carried out the dosage of hemoglobin content, the vessel count, and the concentration of VEGF cytokine, where only the latter parameter showed differences as compared to the control group. The effects of jararhagin-C on tissue fibrogenesis were assessed by dosage of soluble collagen, by histological techniques and the concentration of TGF-β cytokine, we observed an increase in collagen deposition independently of TGF-β. All these factors demonstrate the ability of jararhagin-C to modulate some components of the chronic inflammatory response, as well as events associated with this process.