Anti-inflammatory effects of carvacrol: evidence for a key role of interleukin-10.

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-08T17:50:13Z No. of bitstreams: 1 Lima MS Anti-inflammatory effects....pdf: 662172 bytes, checksum: 5563e5b4c78778c04c1b7009fb92e829 (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-08T17:50:24Z (GMT) No. of bitstreams: 1 Lima MS Anti-inflammatory effects....pdf: 662172 bytes, checksum: 5563e5b4c78778c04c1b7009fb92e829 (MD5)Made available in DSpace on 2014-10-08T18:03:30Z (GMT). No. of bitstreams: 1 Lima MS Anti-inflammatory effects....pdf: 662172 bytes, checksum: 5563e5b4c78778c04c1b7009fb92e829 (MD5) Previous issue date: 2013Universidade Federal da Bahia. Faculdade de Farmácia. Salvador, BA, BrasilUniversidade Federal de Sergipe. Departamento de Fisiologia. São Cristóvão, SE, BrasilUniversidade Estadual de Feira de Santana. Feira de Santana, BA, BrasilHospital São Rafael. Centro de Biotecnologia e Terapia Celular. Salvador, BA, BrasilHospital São Rafael. Centro de Biotecnologia e Terapia Celular. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilUniversidade Federal da Bahia. Faculdade de Farmácia. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilCarvacrol,aphenolicmonoterpene,hasbeenreportedtopossessanti-inflammatoryproperties. However,themechanismsinvolvedinitspharmacologicalpropertiesarecurrentlynotwellunder- stood. Inthepresentstudy,thecontributionofcytokinemodulationtotheanti-inflammatoryeffectsof carvacrolwasinvestigatedinaclassicalinflammationmodel:thecompleteFreund’sadjuvant(CFA)- inducedpawinflammationinmice.Thepawedemawasmeasuredusingaplesthismometer.Pawtissue was removed2haftertheinflammatorystimulustodeterminethelevelsofprostaglandinE2 (PGE2) by enzyme immunoassay,thelevelsofinterleukin-1 b (IL-1b), tumornecrosisfactor-a (TNF-a), and interleukin-10(IL-10)byELISAorthemRNAexpressionofcyclooxygenase-2(COX-2),IL-1b, TNF-a, and IL-10 byreal-timePCR.Administrationofcarvacrolproducedanti-inflammatoryeffectsagainstCFA- inducedinflammationinmice.Treatmentofmicewithcarvacrolat50and100mg/kgattenuatedthe paw edemaandreducedtheIL-1b and PGE2, butnotTNF-a, locallevels.Similarly,carvacrol(100mg/kg) reducedtheCOX-2andIL-1b mRNA expression.ThelevelsofIL-10,ananti-inflammatorycytokine,and the IL-10mRNAexpressionintheinflamedpawwereenhancedbycarvacrol.Inaddition,thetreatment with carvacroldidnotreducetheCFA-inducedpawedemainIL-10knockoutmice.Thepresentresults suggestthatcarvacrolcausesanti-inflammatoryeffectsbyreducingtheproductionofinflammatory mediators,suchasIL-1b and prostanoids,possiblythroughtheinductionofIL-10release

Effect of Combined Application of Dressing Films Based on Mucous Secretion of Achatinafulica and Low Level Laser Therapy on Wound

Abstrac

Evidence for the involvement of descending pain-inhibitory mechanisms in the antinociceptive effect of hecogenin acetate.

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-08T19:20:11Z No. of bitstreams: 1 GAMA K B Evidence for the....pdf: 623352 bytes, checksum: 775057950bf26281a03c9d6374ade542 (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-08T19:20:28Z (GMT) No. of bitstreams: 1 GAMA K B Evidence for the....pdf: 623352 bytes, checksum: 775057950bf26281a03c9d6374ade542 (MD5)Made available in DSpace on 2014-10-08T19:34:21Z (GMT). No. of bitstreams: 1 GAMA K B Evidence for the....pdf: 623352 bytes, checksum: 775057950bf26281a03c9d6374ade542 (MD5) 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