Programa de Pós-graduação em Ciências Biológicas
URI Permanente desta comunidade
Navegar
Navegando Programa de Pós-graduação em Ciências Biológicas por Por Área do CNPQ "CIENCIAS BIOLOGICAS::FISIOLOGIA"
Agora exibindo 1 - 3 de 3
Resultados por página
Opções de Ordenação
Item Avaliação dos efeitos do dipeptídeo aspartato¹-arginina² na próstata ventral de ratos espontaneamente hipertensos(Universidade Federal de Goiás, 2025-03-21) Fernandes, Isadora Garcia; Biancardi, Manoel Francisco; http://lattes.cnpq.br/8810614332757270; Biancardi, Manoel Francisco; Castro, Carlos Henrique de; Sousa, Gessica Coelho deEmbargado.Item Suscetibilidade de fases perinatais no desenvolvimento de doenças cardiometabólicas: a puberdade como período de manifestação de sintomas(Universidade Federal de Goiás, 2023-09-18) Ferreira Junior, Marcos Divino; Matafome, Paulo Nuno Centeio; Custódio, Carlos Henrique Xavier; http://lattes.cnpq.br/0207928273284808; Gomes, Rodrigo Mello; http://lattes.cnpq.br/3121095341590269; Gomes, Rodrigo Mello; Boschero, Antonio Carlos; Mathias, Paulo Cezar de Freitas; Silva, Patrícia Cristina Lisbôa da; Taylor, Paul DavidUnderstanding how susceptibility in the early stages of life can predispose an individual to a greater risk of developing long-term diseases is the focus of DOHaD studies. The main aim of this thesis is to highlight the importance of early assessment of the effects of harmful stimuli suffered in the early stages of life. Given the subtlety of these short-term effects, most studies focus on studying these effects when they have already been consolidated. Here, we open up a new discussion on puberty as the initial period of symptom onset, and also as a favourable time to establish strategies to mitigate the damage already known in adulthood. To this end, we evaluated the effects of maternal exposure to methylglyoxal on metabolic and cardiovascular parameters in young Wistar rat offspring, and also assessed the contribution of growth hormone secretagogue hormone receptor (GHSR) signalling during perinatal stages on neurodevelopment and energy metabolism in young animals. In both studies, the focus was on evaluating several parameters during the pubertal phase. As main findings, we demonstrated that early exposure to glycotoxins led to cardiac and vascular deficiencies, and that modulation of the GHSR receptor in perinatal stages can affect glucose homeostasis. Throughout life, these effects can become more harmful, leading to heart failure or serious metabolic diseases such as non-alcoholic fatty liver disease. This highlights the importance of puberty as a stage for surveillance and intervention.Item Estudo da atividade vasorrelaxante da fração butanólica das folhas de caryocar brasiliense camb. e do ácido gálico em aorta torácica de ratos(Universidade Federal de Goiás, 2015) Oliveira, Lais Moraes de; Filgueira, Fernando Paranaíba; Ghedini, Paulo CésarCaryocar brasiliense Camb., known as pequi, is a typical Brazilian Cerrado tree. Previous study showed that butanolic fraction (BF) of pequi leaves presents endothelium dependent vasorelaxant effect in rat aortic preparations by stimulation of the nitric oxide/guanylyl cyclase (NO/sGC) pathway. In addition, the preliminar chemistry characterization of BF showed the presence of the quercetin and gallic acid phenolic compounds. Considering these informations, the presente study was performed with the aim to identify the mechanisms involved in the activation of NO/sGC pathway by BF and to those involved in the vasorelaxant effect of gallic acid (GA), that it is a compound of BF. The action mechanisms were evaluated on the BF and GA vascular reactivity in the presence of protein agonists and antagonists in isolated preparations of rat thoracic aorta rings. The results of the vascular reactivity were confirmed with the Western blotting technique. In addition, the chemistry characterization of BF was determined with the high-resolution mass spectrometry. The BF promoted vasorelaxant effect in rat thoracic aorta rings in a concentration- dependent manner in preparations with vascular endothelium, which was decreased in the presence of Ca2+/CaM complex inhibitor (calmidazolium) and Pl3-kinase inhibitor (wortmannin). However, the incubation of aortic preparations with KN-93 (Ca2+/CaM dependent protein kinase II inhibitor) and PP2 (Src kinase inhibitor) did not inhibit the vasorelaxation induced by BF. Western blotting tests confirmed that BF caused phosphorylation of eNOS in the Ser1177 residue, effect mediated by the Pl3- kinase/Akt pathway. The chemistry characterization of BF identified the presence of 72 compounds, and the most of them are phenolic compounds and its derivatives. The GA promoted vasorelaxant effect in a concentration-dependent manner in the higher concentrations (0.4-10 mM). The aortic relaxation induced by GA was not abolished by removal of the vascular endothelium. The incubation with the nitric oxide synthase inhibitor (L-NAME), a guanylate cyclase inhibitor (ODQ), or the Ca2+/CaM complex inhibitor (calmidazolium), non-specific potassium channel blocker (TEA), or the blocker voltage-dependent potassium channel (4-aminopyridine) and with the potassium channel blocker type rectifiers (barium chloride) significantly reduced the GA pEC50 values. In addition, GA caused phosphorylation of eNOS in the Ser1177 residue. The results showed that prostanoids vasodilators, Pl3-kinase, Src-Kinase and calcium dependent and sensitive ATP potassium channels are not involved in the vasorelaxant effect promoted by the GA. The incubation with GA promoted reduction of CaCl2-induced contractions and blocked BAY K8644-induced vascular contractions, but it did not inhibit the contraction induced by the release of Ca2+ from the sarcoplasmatic reticulum stores. The results here obtained showed that vasorelaxant effect promoted by FB in aortic rats is due to the phosphorylation of eNOS by Pl3-kinase/Akt pathway and that this effect is caused by the phenolic compounds of BF. On the other hand, the vasorelaxant effect of GA involves endothelium-dependent and -independent mechanisms, as the phosphorylation of eNOS at Ser1177 position and the inhibition of the calcium influx via L-type Ca2+ channels. Taken together, these results help us to understand the action mechanisms involved in the endothelium dependent vasorelaxant effect of BF and for to elucidate the possible compounds associated with this effect. In another way, this study contributes for a better knowledge of the action mechanisms associated with the GA vasorelaxant effect.