| Alzheimer's disease is a senile dementia caused by progressive neurodegeneration of the central nervous system. One of the most prominent pathological characteristics is β-amyloid deposition in senile plaques in the hippocampus. Glucocorticoids are hormones relased during stress and medicine. In plasma sustained glucocorticoids of high concentration can make their access to brain through blood-brain barrier and endanger central nervous system. In central nervous system, hippocampus, a structure possessing high concentration of receptors for glucocorticoids, is likely to be victims of excessive circulating glucocorticoids. At this point, the knowledge about effects of glucocorticoids on β-amyloid-induced hippocampal neurons death is still at the preliminary stage.Objective The objectives of this experiments were to observe insults from dexamethsones and β-amyloid of differernt concentration on hippocampal neurons in vitro. To explore the effect of glucocorticoids on β-amyloid-induced hippocampal neurons death.Methods Primitive hippocampal neurons derived from 18 day embryonic rat were cultured. The cells were respectively exposed to various concentration of dexamethasone (10-5,10-6,10-7,10-8 M ) and β-amyloid (1,5,10,20μM) for 24 hours on its logarithmic growth. In synergistic test the cells were exposed to dexamethasone (10-5,10-6 M) for 24 hours, then β-amyloid (5, 1 μM) respectively were added to the reaction system. Microscopy, MTT assay and the leaking rate of lactate dehydrogenase were used to evaluate changes of celluar morphology and celluar viability. TUNEL was...
|
PDF Full Text Request