Neuroprotective effect of lysophosphatidic acid on AbetaP31-35-induced apoptosis in cultured cortical neurons.
- Author:
Zhao-Qing ZHENG
1
;
Xian-Jun FANG
;
Yu ZHANG
;
Jian-Tian QIAO
Author Information
1. Department of Neurobiology, Shanxi Medical University, Taiyuan 030001, China.
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
antagonists & inhibitors;
Animals;
Animals, Newborn;
Apoptosis;
drug effects;
physiology;
Cells, Cultured;
Cerebral Cortex;
pathology;
Lysophospholipids;
pharmacology;
Mice;
Neurons;
pathology;
Neuroprotective Agents;
pharmacology;
Peptide Fragments;
antagonists & inhibitors
- From:
Acta Physiologica Sinica
2005;57(3):289-294
- CountryChina
- Language:English
-
Abstract:
It has been reported that lysophosphatidic acid (LPA) at its lower concentrations prevents apoptosis induced by serum-deprivation in cultured cortical neurons when LPA is added into the cultural medium with serum withdrawal. The present study was designed to investigate whether LPA could also block the apoptosis induced by beta-amyloid peptide fragment 31-35 (AbetaP31-35) in cultured cortical neurons by using techniques of DNA fragmentation electrophoresis, HO33342 staining, and TUNEL examinations. The results showed that pretreatment of LPA suppressed the AbetaP31-35-induced apoptosis only when LPA was applied to the cultured neurons with lower concentrations (1-10 micromol/L) and especially, with a preceding time of 12-24 h before the AbetaP31-35 exposure. These facts imply that LPA also acts as a neuroprotective factor against AbetaP31-35-induced apoptosis, though the mechanism underlying the protective action in this case may be more complex than that involved in the serum deprivation-induced apoptosis.
