Apoptosis induced by beta-amyloid25-35 in acetylcholinesterase-overexpressing neuroblastoma cells.

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.

• Authors: Hai-Yan Zhang, Stephen Brimijoin, Xi-Can Tang
• Journal: Acta pharmacologica Sinica (Acta Pharmacol Sin) Vol. 24 Issue 9 Pg. 853-8 (Sep 2003) ISSN: 1671-4083 [Print] United States
• PMID: 12956931 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Alkaloids
• Amyloid beta-Peptides
• Cholinesterase Inhibitors
• Neuroprotective Agents
• Peptide Fragments
• Sesquiterpenes
• amyloid beta-protein (25-35)
• huperzine A
• Acetylcholinesterase

Topics

• Acetylcholinesterase (metabolism)
• Alkaloids
• Amyloid beta-Peptides (pharmacology)
• Animals
• Apoptosis (drug effects)
• Cell Survival (drug effects)
• Cholinesterase Inhibitors (pharmacology)
• DNA Fragmentation
• Mice
• Neuroblastoma (pathology)
• Neuroprotective Agents (pharmacology)
• Peptide Fragments (pharmacology)
• Sesquiterpenes (pharmacology)
• Tumor Cells, Cultured