ABSTRACT
Parkinson's disease is a neurodegenerative disorder that affects the central nervous system and is mainly characterized by the loss of dopaminergic neurons and pro-oxidant mechanisms. Eugenol has been widely studied due to its anti-inflammatory and antioxidant activities, making it a promising neuroprotective agent. This study aimed to investigate the effects of eugenol and its combined action with levodopa in the 6-hydroxydopamine-induced Parkinson's disease model. Wistar rats were subjected to intrastriatal injection of 6-hydroxydopamine (21 µg) and then treated with eugenol (0.1, 1, or 10 mg/kg), levodopa (25 mg/kg) or their combination (eugenol 10 mg/kg + levodopa 12.5 mg/kg) orally for 14 days. On the 14th day, the animals were subjected to behavioural tests, and after euthanization and dissection of the brain areas, neurochemical analyses were performed. The results showed that eugenol reduced the oxidative stress and behavioural disturbances induced by 6-hydroxydopamine. The eugenol and levodopa combination was more effective in some behavioural parameters and body-weight gain in addition to promoting an increase in reduced glutathione levels compared to levodopa alone. Thus, the neuroprotective activity of eugenol was observed against motor and neurochemical disorders. Additionally, the eugenol and levodopa combination was promising when compared to conventional treatment.
Subject(s)
Eugenol/pharmacology , Levodopa/pharmacology , Neuroprotective Agents/pharmacology , Parkinson Disease/drug therapy , Animals , Behavior, Animal/drug effects , Body Weight/drug effects , Brain/drug effects , Disease Models, Animal , Glutathione/drug effects , Glutathione/metabolism , Lipid Peroxidation/drug effects , Male , Motor Activity/drug effects , Nitrites/metabolism , Oxidative Stress/drug effects , Oxidopamine/pharmacology , Rats , Rats, WistarABSTRACT
Contaminated eukaryotic cell cultures are frequently responsible for unreliable results. Regulatory entities request that cell cultures must be mycoplasma-free. Mycoplasma contamination remains a significant problem for cell cultures and may have an impact on biological analysis since they affect many cell parameters. The gold standard microbiological assay for mycoplasma detection involves laborious and time-consuming protocols. PCR-based and Bioluminescent assays have been considered for routine cell culture screening in research laboratories since they are fast, easy and sensitive. Thus, the aim of this work is to compare the performance of two popular commercial assays, PCR-based and Bioluminescent assays, by assessing the level of mycoplasma contamination in cell cultures from Rio de Janeiro Cell Bank (RJCB) and also from customers' laboratories. The results obtained by both performed assays were confirmed by scanning electron microscopy. In addition, we evaluated the limit of detection of the PCR kit under our laboratory conditions and the storage effects on mycoplasma detection in frozen cell culture supernatants. The performance of both assays for mycoplasma detection was not significantly different and they showed very good agreement. The Bioluminescent assay for mycoplasma detection was slightly more dependable than PCR-based due to the lack of inconclusive results produced by the first technique, especially considering the ability to detect mycoplasma contamination in frozen cell culture supernatants. However, cell lines should be precultured for four days or more without antibiotics to obtain safe results. On the other hand, a false negative result was obtained by using this biochemical approach. The implementation of fast and reliable mycoplasma testing methods is an important technical and regulatory issue and PCR-based and Bioluminescent assays may be good candidates. However, validation studies are needed.
Subject(s)
Cell Culture Techniques/standards , Luminescent Measurements/methods , Mycoplasma/isolation & purification , Polymerase Chain Reaction/methods , Mycoplasma/genetics , Sensitivity and SpecificityABSTRACT
O autismo é um transtorno mental caracterizado por déficits na socializaçäo, comunicaçäo e imaginaçäo. Em contraste com estas deficiências, as crianças autistas podem apresentar algumas capacidades isoladas especiais denominadas "ilhas de habilidades" como, por exemplo, a facilidade para a aritmética, música e o desenho além de excelente memória fotográfica, memória para dados e detalhes. A co-ocorrência de epilepsia e retardo mental volveu a atençäo dos pesquisadores para as teorias neurobiológicas e cognitivas da síndrome. O presente trabalho propöe um modelo neurobiológico para o autismo baseado no processo biológico fundamental de competiçäo neuronal. Uma rede neuronal artificial capaz de definir mapas corticais - projeçöes sinápticas que preservam vizinhanças entre duas camadas de tecido neuronal - foi projetada para simular o processo de neurodesenvolvimento. Experimentos foram realizados reduzindo-se o nível da substância fator de crescimento neuronal liberada pelos neurônios, resultando em mapas corticais mal desenvolvidos e sugerindo a causa da neurogênese aberrante presente no autismo. As simulaçöes computacionais sugerem que as regiöes do cérebro responsáveis pela formaçäo das representaçöes de mais alto nível estäo malformadas nos pacientes autistas. A perda desta representaçäo integrada do mundo pode resultar em déficits cognitivos específicos na socializaçäo, comunicaçäo e imaginaçäo e pode, também, explicar algumas ilhas de habilidades. O modelo neuronal é baseado em achados biológicos e em teorias cognitivas recentes do autismo. Algumas relaçöes entre as propriedades computacionais do modelo de rede neuronal e a teoria cognitiva do autismo denominada Teoria da Fraca Coerência Central säo estabelecidas, resultando em uma nova visäo para a etiologia do transtorno
Subject(s)
Humans , Male , Female , Child , Adolescent , Adult , Computer Simulation , Cerebral Cortex/embryology , Neural Networks, Computer , Neural Tube Defects , Neurobehavioral Manifestations , Autistic Disorder/diagnosis , Autistic Disorder/etiology , Cognitive ScienceABSTRACT
O autismo e um transtorno mental caracterizado por deficits na socializacao, comunicacao e imaginacao. Em contraste com estas deficiencias, as criancas autistas podem apresentar algumas capacidades isoladas especiais denominadas 'ilhas de habilidades' como, por exemplo, a facilidade para a aritmetica, musica e o desenho alem de execelente memoria fotografica, memoria para dados e detalhes. A co-ocorrencia de epilepsia e retardo mental volveu a atencao dos pesquisadores para as teorias neurobiologicase cognitivas da sindrome. O presente trabalho propoe um modelo neurobiologico para o autismo baseado no processo biologico fundamental de competicao neuronal. Uma rede neuronal artificial capaz de definir mapas corticais - projecoes sinapticas que preservam vizinhancas entre duas camadas de tecido neuronal - foi projetada para simular o processo de neurodesenvolvimento. Experimentos foram realizados reduzindo-se o nivel da substancia fator de crescimento neuronal liberada pelos neuronios, resultando em mapas corticais mal desenvolvidos e sugerindo a causa da neurogenese aberrante presente no autismo. As simulacoes computacionais sugerem que as regioes do cerebro responsaveis pela formacao das representacoes de mais alto nivel estao malformadas nos pacientes autistas. A perda desta representacao integrada no mundo pode resultar em deficits cognitivos especificos na socializacao, comunicacao e imaginacao e pode, tambem, explicar algumas ilhas de habilidades. O modelo neuronal e a teoria cognitiva do autismo denominada Teoria da Fraca Coerencia Central estao estabelecidas, resultando em uma nova visao para a etiologia do transtorno.