DEFAR - Departamento de Farmácia
URI permanente desta comunidadehttp://www.hml.repositorio.ufop.br/handle/123456789/530
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Resultados da Pesquisa
Item Tx2-6 toxin of the Phoneutria nigriventer spider potentiates rat erectile function.(2008) Nunes, Kenia Pedrosa; Gonçalves, Andrey Christian da Costa; Lanza, Luciana Franco; Côrtes, Steyner de França; Cordeiro, Marta do Nascimento; Michael, Richardson; Pimenta, Adriano Monteiro de Castro; Webb, Robert Clinton; Garcia, Maria Elena de Lima PerezThe venom of the spider Phoneutria nigriventer contains several toxins that have bioactivity in mammals and insects. Accidents involving humans are characterized by various symptoms including penile erection. Here we investigated the action of Tx2-6, a toxin purified from the P. nigriventer spider venom that causes priapism in rats and mice. Erectile function was evaluated through changes in intracavernosal pressure/mean arterial pressure ratio (ICP/MAP) during electrical stimulation of the major pelvic ganglion (MPG) of normotensive and deoxycorticosterone-acetate (DOCA)-salt hypertensive rats. Nitric oxide (NO) release was detected in cavernosum slices with fluorescent dye (DAF-FM) and confocal microscopy. The effect of Tx2-6 was also characterized after intracavernosal injection of a non-selective nitric oxide synthase (NOS) inhibitor, L-NAME. Subcutaneous or intravenous injection of Tx2-6 potentiated the elevation of ICP/MAP induced by ganglionic stimulation. L-NAME inhibited penile erection and treatment with Tx2-6 was unable to reverse this inhibition. Tx2-6 treatment induced a significant increase of NO release in cavernosum tissue. Attenuated erectile function of DOCA-salt hypertensive rats was fully restored after toxin injection. Tx2-6 enhanced erectile function in normotensive and DOCA-salt hypertensive rats, via the NO pathway. Our studies suggest that Tx2-6 could be important for development of new pharmacological agents for treatment of erectile dysfunction.Item Angiotensin-converting enzyme inhibition by Brazilian plants.(2007) Braga, Fernão Castro; Serra, Carla Penido; Viana Júnior, Nilton de Souza; Oliveira, Alaíde Braga de; Côrtes, Steyner de França; Lombardi, Júlio AntônioThe potential antihypertensive activity of Brazilian plants was evaluated in vitro by its ability to inhibit the angiotensinconverting enzyme (ACE). Forty-four plants belonging to 30 families were investigated. Plants were selected based on their popular use as antihypertensive and/or diuretics. The following plants presented significant ACE inhibition rates: Calophyllum brasiliense, Combretum fruticosum, Leea rubra, Phoenix roebelinii and Terminalia catappa.Item Validation of a colorimetric assay for the in vitro screening of inhibitors of angiotensin-converting enzyme (ACE) from plant extracts.(2005) Serra, Carla Penido; Côrtes, Steyner de França; Lombardi, Júlio Antônio; Oliveira, Alaíde Braga de; Braga, Fernão CastroAnew method for the in vitro screening of plant extracts with potential angiotensin-converting enzyme (ACE) inhibitory activity is proposed. The method is based on the cleavage of the substrate hippuryl-glycyl-glycine by ACE and subsequent reaction with trinitrobenzenesulfonic acid to form 2,4,6-trinitrophenyl-glycyl-glycine, whose absorbance is determined at 415nm in a microtitre plate reader. Rabbit lung dehydrated by acetone was employed as an enzyme source. Validation of the method showed satisfactory intra-day (CV ¼ 7.63%) and inter-day precision (CV ¼ 13.61%), recovery (97–102.1%), sensitivity (IC50 ¼ 14.1 nmol/l) and linearity in the range 7.5–120 mmol/l of glycyl-glycine (r2 ¼ 0:9921). Besides, the method showed good correlation with a HPLC assay already established for the screening of ACE inhibitors (r ¼ 0:9935 and 0:9034; respectively, for captopril solutions and for plant extracts). The method involves only inexpensive reagents and apparatus.Item ACE inhibition by astilbin isolated from Erythroxylum gonocladum (Mart.) O.E. Schulz.(2010) Lucas Filho, Milton Dayrell; Silva, Grazielle Caroline da; Côrtes, Steyner de França; Guia, Thiago Rennó dos Mares; Ferraz, Vany Perpetua; Serra, Carla Penido; Braga, Fernão CastroErythroxylum species have several traditional uses in different countries, including the treatment of hypertension. The ethanol extract from E. gonocladum aerial parts, a species endemic to the Brazilian cerrado, elicited a concentration-dependent inhibition of angiotensin converting enzyme (ACE) (pIC50=4.53±0.05). Extract fractionation led to the isolation of two compounds, whose structures were assigned by spectrometric data as astilbin and β-sitosterol, along with a mixture of palmitic, stearic and linolenic acids. This is the first report on the occurrence of these compounds on E. gonocladum. Astilbin promoted significant ACE inhibition in vitro (pIC50=5.86±0.33) and its activity did not differ from captopril, when both compounds were assayed at 10 μM concentration.Item Endothelium-dependent vasodilation induced by Hancornia speciosa in rat superior mesenteric artery.(2007) Ferreira, Herick Campos; Serra, Carla Penido; Endringer, Denise Coutinho; Lemos, Virgínia Soares; Braga, Fernão Castro; Côrtes, Steyner de FrançaThe vasodilator effect of the ethanolic extract of leaves from Hancornia speciosa Gomes (HSE) was evaluated in superior mesenteric artery rings. HSE produced a concentration-dependent vasodilation (IC50 ¼ 10.874.0 mg/mL) in arterial rings pre-contracted with phenylephrine, which was completely abolished in endothelium-denuded vessels. Endothelium-dependent vasodilation induced by HSE was strongly reduced by L-NAME (100 mM), a nitric oxide (NO) synthase inhibitor, but neither by atropine, a muscarinic receptor antagonist (1 mM), nor by indomethacin (10 mM), a cyclooxygenase inhibitor. In rings pre-contracted with 80mM KCl, the vasodilator effect of HSE was shifted to the right and was completely abolished in the presence of L-NAME (100 mM). Similar effects were obtained in mesenteric rings pre-contracted with phenylephrine in the presence of KCl 25mM alone or in addition to 100 mM L-NAME.In addition, BaCl2 (1mM) dramatically reduced the vasodilation induced by HSE. Together, these findings led usv to conclude that HSE induces an endothelium-dependent vasodilation in rat mesenteric artery, by a mechanism dependent on NO, on the activation of potassium channels and endothelium-derived hyperpolarizing factor release. Rutin, identified as a major peak in the HPLC fingerprint obtained for HSE, might contribute for the observed vasodilator effect, since it was able to induce an endothelium-dependent vasodilation in rat superior mesenteric arteries.