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J Tradit Chin Med ; 32(4): 646-50, 2012 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-23427404

RESUMEN

OBJECTIVE: To investigate the effect of Bushenyisui Formula on cell apoptosis and positive B cell lymphoma (Bcl-2) in the Brain of rat models of Alzheimer's disease (AD) induced by beta-amyloid protein (Abeta) and the mechanism underlying the effect. METHODS: Total of 40 SD rats, 20 females and 20 males, were randomly assigned to 4 groups, controlled group (A), model group (B), conventional treatment group (C) and Bushenyisui Formula treatment (BYFT) group (D), 10 rats in each group. Abeta 1-42 was injected into the bilateral hippocampus of the rats in group B, C and D to create the models of AD. Sham operation was performed on the rats of group A in the same way by injecting equal volume of 0.9% sodium chloride solution into their bilateral hippocampus. 5 days after operation, Bushenyisui Formula was intraperitoneally administered at a dose of 450 mg/kg to the rats of group D (QD) for 20 days. Equal volume of 0.9% sodium chloride solution was intraperitoneally injected into the rats of group B with the same procedure. C suspension (20 mg/mL) was intraperitoneally injected into the rats of group B with the same procedure. The number of apoptotic cells in Brain and the positive Bcl-2 were counted. The changes of learning and memory abilities were evaluated using Y-maze. RESULTS: Right after the establishment of the models, group B, C and D compared to group A respectively, the outcomes of Y-maze were significantly different from that of group A, which suggested obvious learning and memory disorder in those groups (P < 0.01). After treatment, the times of electronic shocks of group C and D were significantly less than that of group B (P < 0.05), and the numbers of apoptotic cells and positive Bcl-2 were significantly different from those of group B, apoptotic sells' number of group C and D smaller than that of group B and the number of positive Bcl-2 greater than that of group B. CONCLUSION: Bushenyisui Formula could increase the number of Bcl-2 in brain, which improved the function of nervous system pertaining to learning and memory abilities.


Asunto(s)
Enfermedad de Alzheimer/tratamiento farmacológico , Precursor de Proteína beta-Amiloide/toxicidad , Apoptosis/efectos de los fármacos , Encéfalo/citología , Medicamentos Herbarios Chinos/administración & dosificación , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Enfermedad de Alzheimer/genética , Enfermedad de Alzheimer/metabolismo , Enfermedad de Alzheimer/fisiopatología , Precursor de Proteína beta-Amiloide/metabolismo , Animales , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Modelos Animales de Enfermedad , Femenino , Humanos , Masculino , Ratas , Ratas Sprague-Dawley
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