6 research outputs found
Effect of Combined Application of Dressing Films Based on Mucous Secretion of Achatinafulica and Low Level Laser Therapy on Wound
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Evidence for the involvement of descending pain-inhibitory mechanisms in the antinociceptive effect of hecogenin acetate.
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Previous issue date: 2013Universidade Federal da Bahia. Faculdade de Farmácia. Salvador, BA, BrasilUniversidade Federal de Sergipe. Departamento de Fisiologia. Aracaju, SE, BrasilUniversidade Federal de Sergipe. Departamento de Fisiologia. Aracaju, SE, BrasilUniversidade Federal de Sergipe. Departamento de Fisiologia. Aracaju, SE, BrasilUniversidade Estadual de Feira de Santana. Feira de Santana, BA, BrasilUniversidade Estadual de Feira de Santana. Feira de Santana, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil / Hospital São Rafael. Centro de Biotecnologia e Terapia Celular. Salvador, BA, BrasilUniversidade Federal da Bahia. Faculdade de Farmácia. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilHecogenin is a sapogenin present in the leaves of species from the Agave genus, with a wide spectrum of reported
pharmacological activities. The present study was undertaken to evaluate whether hecogenin acetate (1) has antinociceptive
properties and to determine its mechanism of action. The nociceptive threshold was evaluated using the tail flick test in mice.
Mice motor performance was evaluated in a Rotarod test. By using Fos expression as a marker of neural activation, the
involvement of the periaqueductal gray in 1-induced antinociception was evaluated. Intraperitoneal administration of 1 (5−40
mg/kg) produced a dose-dependent increase in the tail flick latency time compared to vehicle-treated group (p < 0.01). Mice
treated with 1 (40 mg/kg) did not show motor performance alterations. The antinociception of 1 (40 mg/kg) was prevented by
naloxone (nonselective opioid receptor antagonist; 5 mg/kg), CTOP (μ-opioid receptor antagonist; 1 mg/kg), nor-BNI (κ-
opioid receptor antagonist; 0.5 mg/kg), naltrindole (δ-opioid receptor antagonist; 3 mg/kg), or glibenclamide (ATP-sensitive K+
channel blocker; 2 mg/kg). Systemic administration of 1 (5−40 mg/kg) increased the number of Fos positive cells in the
periaqueductal gray. The present study has demonstrated for the first time that 1 produces consistent antinociception mediated
by opioid receptors and endogenous analgesic mechanism
KM-34, a Novel Antioxidant Compound, Protects against 6-Hydroxydopamine-Induced Mitochondrial Damage and Neurotoxicity
© 2017 Springer Science+Business Media, LLC, part of Springer Nature The etiology of Parkinson’s disease is not completely understood and is believed to be multifactorial. Neuronal disorders associated to oxidative stress and mitochondrial dysfunction are widely considered major consequences. The aim of this study was to investigate the effect of the synthetic arylidenmalonate derivative 5-(3,4-dihydroxybenzylidene)-2,2-dimethyl-1,3-dioxane-4,6-dione (KM-34), in oxidative stress and mitochondrial dysfunction induced by 6-hydroxydopamine (6-OHDA). Pretreatment (2 h) with KM-34 (1 and 10 μM) markedly attenuated 6-OHDA-induced PC12 cell death in a concentration-dependent manner. KM-34 also inhibited H2O2 generation, mitochondrial swelling, and membrane potential dissipation after 6-OHDA-induced mitochondrial damage. In vivo, KM-34 treatment (1 and 2 mg/Kg) reduced percentage of asymmetry (cylinder test) and increased the vertical exploration (open field) with respect to untreated injure