Abstract
AIM: To examine the relationship between apoptosis induced by β-amyloid fragment 25-35 (Aβ25-35) 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: 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 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 Aβ25-35 was observed when the increased AChE activities were effectively inhibited by huperzine A throughout the 48-h exposure period. CONCLUSION: Although Aβ 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.
Original language | English (US) |
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Pages (from-to) | 853-958+948 |
Journal | Acta Pharmacologica Sinica |
Volume | 24 |
Issue number | 9 |
State | Published - Sep 1 2003 |
Keywords
- Acetylcholinesterase
- Amyloid beta protein
- Apoptosis
- SC35 cells
- SC42 cells
ASJC Scopus subject areas
- Pharmacology
- Pharmacology (medical)