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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
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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
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Objective:To construct a eukaryotic expression plasmid pcDNA3.1(-)-Humanin.Methods:The recombinant plasmidpGEMEX-1-Humanin was digested with restriction endonucleases BamH Ⅰ and Hind Ⅲ and the Humanin gene fragments,about100 bp length,were obtained.Then the Humanin gene fragments were inserted into eukaryotic expression vector pcDNA3.1(-)andthe recombinant plasmids pcDNA3.1(-)-Humanin were identified by sequencing.Results:Recombinant plasmid DNA success-fully produced a band which had the same size as that of the thimauin positive control.The sequence of recombinant plasmidsaccorded with the Humnain gene sequence.Conclusions:A eukaryotic expression plasmid of Humanin was successfully con-structed. 相似文献
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Study of apolipoprotein E genetic polymorphism in patients with atherosclerotic cerebral infarction 总被引：1，自引：0，他引：1
INTRODUCTIONAtheroscleroticCerebralInfarction (ACI)isoneofthemostcommoncerebralvasculardis easse.Itspathogenesishasnotyetbeencom pletelyexpounded ,althoughmoreandmorestudiesshowingthatgeneticfactorsmayplayanimportantrole ,especiallygeneticmutations.Lo cat… 相似文献
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Objective: To explore the frequency and significance of ApoE gene polymorphisms in Chinese patients with atherosclerotic cerebral infarction (ACI). Methods: Polymerase chain reaction and gene sequencing, single nucleotide polymorphisms of ApoE gene were used to analyze 33 cases of patients with ACI and 35 controls. Results: The frequencies of ApoE gene single nucleotide polymorphisms 465C/G, 462C/G and 451delC in the ACI group were significantly higher than those in the control group (P<0.05). The prevalence of polymorphism 486G/T in the control group was significantly higher than that in the ACI group (P=0.011). Conclusions: 465C/G,462C/G and 451delC polymorphisms might be associated with ACI.486GT allele might have protective effect on the pathogenesis of ACI. 相似文献
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