Navegando por Assunto "Nimesulida"

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Acesso aberto (Open Access)
Atividade antifúngica da nimesulida isolada ou em associação com a terbinafina contra fungos dermatófitos e seu provável mecanismo de ação in vitro
(Universidade Federal do Pará, 2015) MATOS, Rafaelle Fonseca de; MONTEIRO, Marta Chagas; http://lattes.cnpq.br/6710783324317390
The dermatophytes has shown resistance to current antifungal agents such as Terbinafine, and this has led to research into new compounds as an alternative therapy. Thus, this study evaluated the action of non-steroidal antiinflamatory (NSAIDs) Nimesulide isolated and combined with Terbinafine against dermatophytes, dependence on Prostaglandins this mechanism of action and the effect of Nimesulide in the production of urease and fungal viability. The tests based were on CLSI, clinical and laboratory standards institute - reference method for microdilution test ground for antifungal susceptibility against filamentous fungi (M38-A standard). For clinical isolates of the species Trichophyton mentagrophytes, Trichophyton rubrum, Epidermophyton floccosum and Microsporum canis, the minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) varied in the range> 400 ug / ml -> 0.112 g / ml. However, the results showed that the concentration of 0.002 mg / ml of Nimesulide was able to inhibit the growth of T. mentagrophytes ATCC 9533 and the concentration of 0.008 mg / ml was fungicidal for the same strain. Same values were find for Terbinafine on this strain. The inhibition of fungal growth by Nimesulide was reverse with application of exogenous prostaglandin E2 (PGE2). The urease test showed that T. mentagrophytes ATCC 9533 produces the enzyme, but no inhibition of fungal viability. In the nimesulide / Terbinafine association inhibition occurred in a ratio of 9: 1, or 0.0002 g / ml of Terbinafine and 0.0018 ug / ml of Nimesulide inhibited fungal growth but this result was the indifferent Fractional inhibition index. Nimesulide showed antifungal activity against dermatophytes in low concentrations, but other studies must be performed with the aid of molecular modeling to improve the targeting compound.
Acesso aberto (Open Access)
Inibição de ciclooxigenase-2 (COX-2) em camundongos infantis saudáveis: consequências sobre o comportamento e o perfil oxidativo
(Universidade Federal do Pará, 2022-08-26) LIMA, Klinsmann Thiago; BASTOS, Gilmara de Nazareth Tavares; http://lattes.cnpq.br/2487879058181806
In the central nervous system, cyclooxygenase 2 (COX-2) is a constitutive enzyme, expressed by neurons from different brain regions, which acts in the maintenance of neural homeostasis, modulating synaptic plasticity and the generation of new neurons. Non-steroidal anti-inflammatory drugs (NSAIDs) are drugs of choice that act to inhibit COX enzymes, with nimesulide (NMS) being a drug of this class. Several studies have demonstrated the role of these enzymes in neurological and neuropsychiatric disorders such as Parkinson's Disease, Alzheimer's Disease, epilepsy, depression and schizophrenia. Thus, the aim of the present work was to investigate the effects of COX- 2 inhibition in healthy infant mice on behavioral and biochemical criteria, using NMS as a pharmacological blockade tool. For this, male Swiss infant mice, aged between 21 and 34 days, were used. The animals were randomly divided into four groups: (1) Vehicle, (2) NMS 2.5mg/kg, (3) NMS 5mg/kg and (4) NMS 10mg/kg. Two injections of NMS/Vehicle were administered intraperitoneally daily. Throughout the experiment, the body mass of the animals was recorded daily and they were subjected to behavioral tests: open field test (OFT), elevated plus maze (EPM), light/dark box test (LDBT) and novel object recognition test (NORT). In addition, brain samples were collected for biochemical analyses. The results demonstrated the induction of oxidative stress with increased levels of lipid peroxidation in the cortex and hippocampus, as well as the expression of an anxiogenic behavior, observed in the EPM, possibly potentiated by fear. In the NORT, the animals of the NMS 5mg/kg group showed a deficit in the memory of recognizing new objects, and consequently, in the short-term memory. Thus, our results demonstrated that the in vivo inhibition of COX-2 in infant animals induces an anxious-like behavior possibly potentiated by fear, but does not affect the exploration and locomotion of these animals. Furthermore, COX-2 inhibition induced cortical and hippocampal oxidative stress. Therefore, the inhibition of COX-2 in infantile and non-inflamed animals may compromise cognitive functions such as memory and learning, as well as alter the cerebral oxidative profile.