Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Chin Med J (Engl) ; 125(21): 3875-9, 2012 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-23106891

RESUMO

BACKGROUND: Proneurotrophins such as the precursor of nerve growth factor (proNGF) and the precursor of brain-derived neurotrophic factor (proBDNF) interacted with sortilin and p75(NTR) to form a complex capable of activating an apoptotic signaling. We found that the expression of p75(NTR) and sortilin was increased in ischemic retina induced by elevated intraocular pressure (IOP), but the protein expression changes of proNGF and proBDNF in the same situation were not clear. This study aimed to ascertain the protein expression changes of proNGF and proBDNF in ischemic retina induced by elevated IOP. METHODS: Expression of proBDNF and proNGF was examined by double-labeling immunochemistry in normal rat retina, examined using Western blotting and analyzed using statistical methods in ischemic retina induced by elevated IOP. RESULTS: Immunocytochemistry showed that the proBDNF expressed in the ganglion cell layer (GCL) while the proNGF primarily existed in both the nerve fiber layers (NFL) and large ganglion cell bodies of normal rat retina. Western blotting analysis demonstrated that the molecule weights of 28 kD (proBDNF)/25 kD (proNGF) band were increased significantly (P < 0.05) at days 3, 5 and 7 after retinal elevated-IOP-induced ischemia. CONCLUSION: ProBDNF expressed in the GCL and proNGF primarily presented in NFL and large ganglion cell bodies of normal rat retina, the protein expression forms of 28 kD proBDNF and 25 kD proNGF increased in ischemic retina induced by elevated IOP.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/análise , Pressão Intraocular/fisiologia , Isquemia/metabolismo , Fator de Crescimento Neural/análise , Precursores de Proteínas/análise , Doenças Retinianas/metabolismo , Animais , Western Blotting , Imuno-Histoquímica , Masculino , Ratos , Ratos Wistar
2.
Brain Res ; 1106(1): 30-39, 2006 Aug 23.
Artigo em Inglês | MEDLINE | ID: mdl-16843444

RESUMO

The proliferative activity of neural precursors from the subventricular zone (SVZ) was investigated after a unilateral lesion was formed in the nigrostriatal pathway in adult rats. The lesion was formed by unilateral injection of 6-hydroxydopamine (6-OHDA) into the nigrostriatal pathway, and then bromodeoxyuridine (BrdU) was injected (ip) for 4 days or 2 weeks 10 days after the lesion was formed. The rats were killed, and the brain sections were immunohistochemically stained to detect the expression of BrdU, polysialylated neural-cell-adhesion molecule (PSA-NCAM), glial fibrillary acidic protein (GFAP) and tyrosine hydroxylase (TH) in the SVZ and the striatum (STR). The results showed that the BrdU(+) cells increased significantly in the SVZ, ipsilateral to the lesion at 2 weeks after the lesion. The PSA-NCAM(+) and GFAP(+) cells were also increased in the SVZ at this time. Some BrdU-labeled cells were seen in the same side of the STR and were double-labeled with PSA-NCAM. These cells had a tendency to migrate from the SVZ to the STR. The number of positive cells decreased at 4 weeks after the lesion was formed. The number of nigrostriatal projections with TH(+) decreased significantly in the STR on the lesion side, and the level of decrease was related to the quantity of BrdU-labeled cells at 2 weeks. These results indicate that the neural precursors in the SVZ of adult rats may increase after a lesion has been formed in the nigrostriatal pathway, and these cells might migrate into the STR on the same side.


Assuntos
Proliferação de Células/efeitos dos fármacos , Corpo Estriado/fisiologia , Regeneração Nervosa/fisiologia , Plasticidade Neuronal/fisiologia , Transtornos Parkinsonianos/fisiopatologia , Células-Tronco/fisiologia , Animais , Biomarcadores/metabolismo , Bromodesoxiuridina , Movimento Celular/efeitos dos fármacos , Movimento Celular/fisiologia , Corpo Estriado/citologia , Corpo Estriado/efeitos dos fármacos , Denervação , Modelos Animais de Doenças , Proteína Glial Fibrilar Ácida/metabolismo , Masculino , Degeneração Neural/induzido quimicamente , Degeneração Neural/fisiopatologia , Molécula L1 de Adesão de Célula Nervosa/metabolismo , Vias Neurais/efeitos dos fármacos , Vias Neurais/patologia , Vias Neurais/fisiopatologia , Oxidopamina , Ratos , Ratos Sprague-Dawley , Recuperação de Função Fisiológica/fisiologia , Ácidos Siálicos/metabolismo , Células-Tronco/citologia , Células-Tronco/efeitos dos fármacos , Substância Negra/efeitos dos fármacos , Substância Negra/patologia , Substância Negra/fisiopatologia , Tirosina 3-Mono-Oxigenase/metabolismo , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/fisiologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...