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SourceAvailable from: ftp.benthamscience.com[Show abstract] [Hide abstract]
ABSTRACT: We evaluated the neuropharmacological profile of acetylated alpha-and beta-amyrin (AcAMY) obtained by the acetylation of the isomeric mixture of alpha-and beta-amyrin isolated from Protium heptaphyllum. Male Swiss mice were administered with AcAMY (2.5, 5, 10 and 25 mg/kg, i.p.), and anticonvulsant (pentylenetrazole-and pilocarpine-induced convulsions), sedative (barbiturate-induced sleep and open field tests) and anxiolytic (elevated plus maze test) activities were studied. Results showed that AcAMY administered intraperitoneally or orally, protected the animals against penty-lenetetrazole-but not against pilocarpine-induced convulsions. The drug increased both the latency to the 1 st convulsion and the latency to death. The barbiturate-induced sleeping time was also increased, as well as the ethyl ether-induced sleeping time, confirming the sedative nature of AcAMY. The acute administration of AcAMY also produced an anx-iolytic effect. After the sub-chronic administration, both sedative and anxiolytic effects were manifested, at the two higher doses. Amino acids measurements in brain areas of mice treated with AcAMY (25 mg/kg, i.p., for 7 days) showed an 89% increase in tyrosine levels, in the hippocampus. In the striatum, tyrosine and taurine were increased by 97 and 79%, re-spectively, while decreases in the levels of aspartate, GABA and glutamate of 72, 55 and 60%, respectively were ob-served. In conclusion, our results showed that AcAMY presents sedative, anxiolytic and anticonvulsant properties. Al-though the drug mechanism of action is not completely clarified, it seems to involve a decrease in excitatory amino acids and an increase of inhibitory amino acids. Furthermore, the GABAergic system may also play a role.The Open Pharmacology Journal 11/2014; DOI:10.2174/1874143600903010009
Conference Paper: PERDAS NAS OPERAÇÕES PRÉ-ABATE: ÊNFASE EM ESPERA[Show abstract] [Hide abstract]
ABSTRACT: Introdução Dentre as poucas informações existentes sobre as operações pré-abate, sabe-se que muitos são os fatores que contribuem com o estresse das aves durante estas etapas e que a intensidade destes efeitos determina o nível elevado de perdas por mortalidade na chegada ("Death on arrival" – DOA). No entanto, a busca pela localização destes pontos críticos tornou-se um dos principais desafios da cadeia produtiva de frangos de corte, com o objetivo de reduzir as perdas nesta fase, e consequentemente aumentar a lucratividade para todos os atores envolvidos no cenário avícola. Destaca-se nesta abordagem a operação de espera nos abatedouros, que consiste no momento em que as aves aguardam na carga o momento de abate. Esta etapa é uma das mais importantes e decisivas quanto ao sucesso obtido entre a retirada das aves das granjas e sua chegada à linha de abate, dentro de condições que facilitem a comercialização de um produto final de qualidade superior. Todavia, mesmo com todos os cuidados tomados nas etapas de pega, carregamento e transporte, estes podem ser perdidos em poucas horas durante a espera, caso esta seja mal planejada para o objetivo de oferecer um ambiente térmico adequado para os animais. Pouco se sabe das condições ideais que possam contribuir para a redução da carga de estresse do animal, proveniente das etapas anteriores.AVESUI'09; 09/2014
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ABSTRACT: Our previous findings enable us to hypothesize that the sesquiterpene (-)-α-bisabolol acts as inhibitor of voltage-dependent Ca(2+) channels in smooth muscle cells. The current study was aimed at consolidating such hypothesis through the recording of isometric tension in isolated aortic preparations, measurement of intracellular Ca(2+) by imaging technique as well as discovery of channel target using in silico analysis method. In rat aortic rings, (-)-α-bisabolol (1-1000μM) fully relaxed KCl- and phenylephrine-elicited contractions, but the IC50 values to produce such effects differed significantly (22.8 [17.6-27.7] and 200.7 [120.4-334.6] μM, respectively). Its ability to relax phenylephrine-induced contractions remained unaffected by L-NAME, indomethacin, 1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one, tetraethylammonium, glibenclamide or KT-5720. Under Ca(2+)-free conditions, (-)-α-bisabolol (100μM) did not alter the contractions evoked by phenylephrine or caffeine whereas it reduced those evoked by CaCl2 in KCl-, but not in PHE (in the presence of nifedipine)-stimulated preparations. (-)-α-Bisabolol did not significantly alter the contractions induced by the extracellular Ca(2+) restoration in cyclopiazonic acid-treated aortic rings or those evoked by phorbol 12,13-dibutyrate. In mesenteric artery rings loaded with Fluo-4AM, simultaneous measurement of force and cytosolic Ca(2+) revealed that (-)-α-bisabolol blunted the cytosolic levels of Ca(2+) in response to K(+) but not to norepinephrine. Silico docking analysis of the Cavβ2a subunit of voltage-dependent Ca(2+) channel indicated the existence of putative docking sites for (-)-α-bisabolol. The findings from confocal imaging and in silico analysis reinforce the ability of (-)-α-bisabolol to inhibit preferentially contractile responses evoked by Ca(2+) influx through voltage-dependent Ca(2+) channels.Vascular Pharmacology 08/2014; DOI:10.1016/j.vph.2014.06.006
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