排序方式： 共有2条查询结果，搜索用时 0 毫秒
1
1.
Objective: To construct a PC12 cell strain with neuronal differentiation, and observe the apoptosis and pro-liferation activity effects induced these cells by Amyloid beta-Protein (Aβ-43). Methods: 1) PC12 cells in logarithmicgrowth phase were subcultured for 24 h. After the culture fluid was changed, the cells were treated with Rat-β-NGF andcultured for 9 days. 2) Neuronal differentiation of PC12 cells in logarithmic growth phase were divided into four groups:control group (0), experimental group (1), experimental group (2) and experimental group (3). The concentrations of Aβ inthe four groups were 0 μmol/L, 1.25 μ mol/L, 2.5 μ mol/L and 5 μmol/L, respectively. The cells were harvested at 24, 48 and72 h later and stained with AnnexinV-FITC/PI after centrifugation and washing. Then flow cytometry was conducted toexamine the apoptosis percentage. 3) NGF-induced PC12 cells were selected and Aβ with different concentrations wasadded. The final concentrations of Aβ were 0 μmol/L, 1.25 μmol/L, 2.5 μmol/L and 5 μ mol/L, respectively. After the cellswere incubated in an atmosphere of 5% CO2 at 37 ℃ in an incubator for 72 h, the OD values were examined. Results: 1)Neuronal differentiated PC 12 cell lines were successfully established. 2) Flow cytometric examination indicated that Aβ(1.25, 2.5, and 5.0 μmol/L) could effectively induce apoptosis of neuronal-differented cells at the 24 h, 48 h and 72 h timepoints. 3) Aβ (0-5.00 μ mol/L) had no obvious effect on proliferation or restraining of the neuronal differentiation of thePC 12 cells after a 72 h interacting process. Conclusion: This investigation revealed successful neuronal differentiation of thePC12 cell strain. The induction of apoptosis of the neurocytes by various concentrations of Aβ was observed and the in-fluence of Aβ on induced proliferation of PC 12 cells by Rat-β-NGF was revealed. This study -05 provide basis for futureresearch on the molecular cure of AD and interdiction of AD evolution. 相似文献
2.
INTRODUCTION Senile dementia of the Alzheimer type calledin short Alzheimer’s Disease (AD), is the mostcommon type of senile dementia. The pathologicalcharacters of AD are neuron loss, accumulation of senile lipofuscin pigment (SP) caused by the ex- tracellular deposition of Amyloid beta-Protein (Aβ) and neurofibrillary tangles (NFT) caused by ac-t cumulation of excessively … 相似文献
1