Pituitary adenylate cyclase activating polypeptide protects neuro-2a cells from beta amyloid protein cytotoxicity by modulating intracellular calcium.
- Author:
Lan-Run GUI
1
;
Yan ZHOU
;
Bing-Lie ZHANG
;
Wen-Bin LI
Author Information
1. Institute of Microbiology, Beijing Military Medical College, Beijing 100071. guilanrun@hotmail.com
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
antagonists & inhibitors;
toxicity;
Calcium;
metabolism;
Calcium Channels;
metabolism;
Cell Line, Tumor;
Humans;
Neuroblastoma;
pathology;
Neuroprotective Agents;
pharmacology;
Pituitary Adenylate Cyclase-Activating Polypeptide;
pharmacology
- From:
Acta Physiologica Sinica
2003;55(1):42-46
- CountryChina
- Language:Chinese
-
Abstract:
MTT analysis and intracellular calcium measurement by using confocal laser scanning microscopy were used to study the possible mechanism of protective effect of pituitary adenylate cyclase activating polypeptide 27 (PACAP27) from beta amyloid protein (Abeta)-induced neurotoxicity. The results showed that treatment with PACAP (less than 0.1 micromol/L) increased the survival and reproductive ability of neuro-2a cells and protected the neuro-2a cells from being injured by Abeta. The protective effect of PACAP27 was reversed by the competitive PACAP receptor antagonist PACAP6-27. An increase in intracellular calcium was observed when the cells were challenged with Abeta and PACAP. But the calcium increase induced by Abeta kept stable for a long time while PACAP caused a transient rise in intracellular calcium. The intracellular calcium increase induced by Abeta was blocked by pretreatment with PACAP for 10 min. It is suggested that the neuroprotective effect of PACAP against neuronal damage induced by Abeta may result from its role in inhibiting the sustained rise in intracellular calcium.
