Investigação da atividade vascular do extrato, frações e compostos isolados das folhas de Plinia cauliflora (Myrtaceae) em aorta de camundongo

• Ano de defesa: 2018
• Autor(a) principal: Walma Pereira de Vasconcelos
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; Brasil; ICB - INSTITUTO DE CIÊNCIAS BIOLOGICAS; Programa de Pós-Graduação em Ciências Biológicas - Fisiologia e Farmacologia; UFMG
• Palavras-chave em Português: Plínia cauliflora; Jabuticaba; Vasodilatação; Óxido nítrico; Farmacologia; Myrtaceae
• Link de acesso: http://hdl.handle.net/1843/35676

Introduction:Plinia cauliflora Kausel (Myrtaceae) known as “jabuticaba” is an edible plant native from Brazil. Its fruits are rich in polyphenolic compounds and have been described as hypotensive in rats. The leaves of P. cauliflora are also rich in polyphenolic compounds, but their effect in the cardiovascular system is still unknown. Therefore, the present study aimed at investigating the vasodilator effect of the polyphenolic-rich hydroalcoholic extract (EHA), aqueous (FA) and butanol (FB) fractions obtained of the leaves from Plinia cauliflora in mice aorta. Methods: All protocols were approved by CEUA/UFMG (#218/2017). Male Swiss mice (10-12 weeks) were euthanized by decapitation. Aortic rings were obtained and kept in an organ bath system containing Krebs at 37°C, gassed with 95% O2 and 5% CO2, and maintained at a tension of 0.5g. Systolic blood pressure (SBP) of normotensive mice was measured by tail-cuff pletismography. The FA (10 and 30 mg/kg) was given intraperitoneally, single dose, in respective group of mice, and the SBP was monitored for 2 h. Results and discussion: In aortic rings pre-contracted with phenylephrine, EHA, FA, and FB induced a concentration- and endothelium-dependent vasodilatation. The pre-incubation with L-NAME (300 μM), a non-selective inhibitor of nitric oxide synthase (NOS), abolished the vasodilatation of FA. In addition, wortmannin (30nM), a selective inhibitor of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), significantly shifted the concentration-response curve to the right and reduced the maximal effect of FA. In the presence of TRIM (300μM), a selective inhibitor of neuronal NOS (nNOS), the vasodilator effect of FA was not changed. Finally, in the presence of ODQ (10 μM), a selective inhibitor of the soluble guanylyl cyclase (sGC), the vasodilatation effect of FA was abolished. In vivo experiments, FA was able to induce a dose-dependent hypotensive effect in normotensive mice, with maximum response at 60 minutes. Conclusions: Altogether, these results suggest that the EHA, FA and FB promote an endothelium-dependent vasodilator effect. The vasodilation effect of FA involves the participation of the NO pathway. Furthermore, the FA was able to induce a hypotensive effect in normotensive mice