| Apoptosis induced by β-amyloid25-35 in acetylcholinesteraseoverexpressing neuroblastoma cells |
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| 引用本文： | Zhang HY,Brimijoin S,Tang XC. Apoptosis induced by β-amyloid25-35 in acetylcholinesteraseoverexpressing neuroblastoma cells[J]. Acta pharmacologica Sinica, 2003, 24(9): 853-858 |
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| 作者姓名： | Zhang HY Brimijoin S Tang XC |
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| 摘 要： | AIM: To examine the relationship between apoptosis induced by β-amyloid fragment 25-35 (Aβ25-35) and the activ-ity of acetylcholinesterase (ACHE) in AChE over-expresser-SC42 cells. METHODS: Cell survival was measuredby microscopy and MTT reduction; DNA laddering was observed by electrophoresis; AChE activity was determined by spectrophotometry. RESULTS: Aβ25-35 1 μmol/L exposure for 24-48 h caused a significant decrease in cell viability, along with changes in morphology and DNA fragmentation. AChE activity was affected in an inversemanner, increasing gradually to a level that was 1.7-fold higher than control at the 48-h time point. No change in thecytotoxicity of Aβ25-35 was observed when the increased AChE activities were effectively inhibited by huperzine Athroughout the 48-h exposure period. CONCLUSION: Although Aβ25-35 can induce apoptosis in SC42 cells andsimultaneously increase AChE activity, the capacity of AChE to hydrolyze acetylcholine is not involved in thisapoptosis model.
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| 关 键 词： | Aβ25-35 乙酰胆碱酶 神经细胞瘤 细胞凋亡 MTT法 阿海默滋疾病 |
Apoptosis induced by beta-amyloid25-35 in acetylcholinesterase-overexpressing neuroblastoma cells |
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| Zhang Hai-Yan,Brimijoin Stephen,Tang Xi-Can. Apoptosis induced by beta-amyloid25-35 in acetylcholinesterase-overexpressing neuroblastoma cells[J]. Acta pharmacologica Sinica, 2003, 24(9): 853-858 |
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| Authors: | Zhang Hai-Yan Brimijoin Stephen Tang Xi-Can |
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| Affiliation: | [1]StateKeyLaboratoryofDrugResearch,ShanghaiInstituteofMateriaMedica,ShanghaiInstitutesforBiologicalSciences,ChineseAcademyofSciences,Shanghai201203,China [2]DepartmentofMolecularPharmacology,MayoClinic,200FirstStSW,RochesterMN55905,USAProfTANGXi-Can.Fax86-21-5080-7088.E-mailxctang@mail.shcnc.ac.cn;andProfStephenBRIMIJOIN.Fax507-284-9111,E-mailbrimijoi@mayo.edu [3]ProfTANGXi-Can.Fax86-21-5080-7088.E-mailxctang@mail.shcnc.ac.cn;andProfStephenBRIMIJOIN.Fax507-284-9111,E-mailbrimijoi@mayo.edu |
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| Abstract: | AIM: To examine the relationship between apoptosis induced by beta-amyloid fragment 25-35 (A beta 25-35) and the activity of acetylcholinesterase (AChE) in AChE over-expresser--SC42 cells. METHODS: Cell survival was measured by microscopy and MTT reduction; DNA laddering was observed by electrophoresis; AChE activity was determined by spectrophotometry. RESULTS: A beta 25-35 1 micromol/L exposure for 24-48 h caused a significant decrease in cell viability, along with changes in morphology and DNA fragmentation. AChE activity was affected in an inverse manner, increasing gradually to a level that was 1.7-fold higher than control at the 48-h time point. No change in the cytotoxicity of A beta 25-35 was observed when the increased AChE activities were effectively inhibited by huperzine A throughout the 48-h exposure period. CONCLUSION: Although A beta 25-35 can induce apoptosis in SC42 cells and simultaneously increase AChE activity, the capacity of AChE to hydrolyze acetylcholine is not involved in this apoptosis model. |
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