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1.
Journal of Gorgan University of Medical Sciences. 2012; 14 (3): 10-18
in Persian | IMEMR | ID: emr-155572

ABSTRACT

Research have been focused on the applying the chemical inducer for transdifferentiation the adult BMSCs into neural cell. So that, at the first should investigate the toxcity effect of the chemical inducer on the induced cells. Plasticity and easy accessibility of bone marrow mesenchymal stem cells is a unique charactristic for treatment of neural disorderies. This study was desgined to determine the inductive effect of Deprenyl and Dimethyl sulfoxide on proliferation and survival of the mesenchymal stem cells. In this experimental study, BMSCs isolated from the adult rat bone marrow and cultured in alpha MEM containing 10% FBS. Cell identity for surface antigens was performed in third passage by immunocytochemistry and multipotancy capacity of BMSCs was done by BMSC differentiation into adipocytes and osteocytes. The cells were exposed to chemical agents [a: the alpha MEM medium supplemented with 2% DMSO, b: the alpha MEM medium supplemented with 10[-8]M Deprenyl] for 24 hours and then transferred to alpha MEM containing 10% FBS cell survival and proliferation was evaluated after the 24, 48, 72 and 96 houres by MTT [3-[4-5-Dimethylthiazolyl-2-y1]-2,5-diphenyltetrazolium romid] test. Data were analyzed using SPSS-16, One-Way ANOVA and Tukey tests. In addition to expression the surface antigens and adipogenic and osteogenic differentiation by BMSCs, MTT test results showed that proliferation and survival of induced-deprenyl and DMSO cells within 48, 72 and 96 hours after the induction was increased significantly than negative control group. Deprenyl increases survival and cell proliferation compared to Dimethyl Sulfoxide. It can be used as cell inducer


Subject(s)
Animals, Laboratory , Selegiline/pharmacology , Dimethyl Sulfoxide/pharmacology , Bone Marrow , Rats , Cell Proliferation , Cell Survival
2.
Neurobiologia ; 60(1): 13-20, jan.-mar. 1997.
Article in Portuguese | LILACS | ID: lil-242579

ABSTRACT

A doença de Parkinson foi descrita em 1817 e desde então os conhecimentos sobre sua patologia e formas de tratamento foram crescendo. A levodopaterapia constituiu um avanço significativo no tratamento sintomático desta doença. Os estudos sobre os possíveis mecanismos etiopatogênicos da doença de Parkinson (DP) formaram a base para proposição de um novo tipo de abordagem terapêutica: um tratamento possivelmente curativo ou neuroprotetor. Neste trabalho é feita uma revisão do uso do deprenil e tocoferol (Vit E) nas fases iniciais da DP. Os resultados mostraram que o tocoferol não apresentou efeito terapêutico e que o efeito do deprenil ainda não foi definido se neuroprotetor, sintomático ou ambos


Subject(s)
Parkinson Disease/therapy , Levodopa/pharmacology , Selegiline/pharmacology , Vitamin E
3.
Folha méd ; 109(3): 85-90, set. 1994.
Article in Portuguese | LILACS | ID: lil-159164

ABSTRACT

O parkinsonismo idiopático (doença de Parkinson) e secundário, ou seja, que apresenta etiologia conhecida (pós-encefalítico, por toxinas, por drogas ou por algumas doenças degenerativas) såo processos neurodegenerativos que afetam progressivamente as funçÆes motoras normais do indivíduo. Neste trabalho, os aspéctos clínicos, etiológicos, fisiopatológicos e principalmente a descriçåo do arsenal farmacológico e as medidas utilizadas no combate ou retardo medicamentoso do parkinsonismo såo abordados e discutidos


Subject(s)
Humans , Amantadine/pharmacokinetics , Amantadine/pharmacology , Bromocriptine/pharmacokinetics , Bromocriptine/pharmacology , Carbidopa/pharmacokinetics , Carbidopa/pharmacology , Parkinson Disease/etiology , Parkinson Disease/physiopathology , Parkinson Disease/therapy , Levodopa/pharmacokinetics , Levodopa/pharmacology , Selegiline/pharmacokinetics , Selegiline/pharmacology
7.
Indian J Exp Biol ; 1990 Aug; 28(8): 742-5
Article in English | IMSEAR | ID: sea-56965

ABSTRACT

Effects of a selective monoamine oxidase (MAO)--A inhibitor, clorgyline, a selective MAO-B inhibitor, deprenyl, and a non-selective MAO inhibitor, nialamide, were investigated on footshock-induced aggression (FIA) in paired rats. The doses and pretreatment times of the inhibitors used were based on an earlier reported in vivo dose-response and time-course study. In addition, apomorphine, a dopaminergic receptor agonist, and beta-phenylethylamine, a preferred substrate for MAO-B, were also used to garner corroborative evidence. The results of the study indicate that selective MAO-A inhibitors are likely to attenuate FIA by augmenting central serotonergic activity, while selective MAO-B inhibitors accentuate the behaviour by facilitating dopaminergic activity. A permissive role for noradrenaline could not be delineated by the available data.


Subject(s)
Aggression/drug effects , Animals , Apomorphine/pharmacology , Clorgyline/pharmacology , Female , Male , Monoamine Oxidase/classification , Nialamide/pharmacology , Pain , Rats , Rats, Inbred Strains , Selegiline/pharmacology
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