Relationship between amyloid beta-protein and oxidative stress and the protective role of pituitary adenylate cyclase activating polypeptide against oxidative stress induced damage on neuro-2a cells.
- Author:
Lan-Run GUI
1
;
Bing-Lie ZHANG
;
Zheng-Yu FANG
;
Wen-Bin LI
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; toxicity; Apoptosis; Cell Survival; Cells, Cultured; Humans; Hydrogen Peroxide; pharmacology; Neurons; cytology; drug effects; Oxidative Stress; Pituitary Adenylate Cyclase-Activating Polypeptide; pharmacology
- From: Chinese Journal of Applied Physiology 2003;19(2):171-174
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo observe the relationship between amyloid beta-protein (Abeta) and oxidative stress and the protective role of pituitary adenylate cyclase activating polypeptide (PACAP, PACAP-27) against damage induced by oxidative stress (H2O2) in neurem-2a cells.
METHODSWith cultured neuro-2a cells the cell survival and apoptosis were measured by MTT assay, Hoechest33258 staining, DNA ladder and the percentage of small DNA fragment.
RESULTSConcentration-dependent toxicity was induced with H2O2 treatment for 24 h. The neurotoxicity of H2O2 was increased by about 10 times with cotreatment neurons with amyloid beta-protein fragment 25-35 (Abeta(25-35)). While decrease the percentage of small DNA fragmentation the cell survival was increased with co-treatment with PACAP-27(which were added to the culture everyday). The effect of PACAP was not reversed with antagonist of PACAP receptor, PACAP(6-27).
CONCLUSIONAbeta and H2O2 can promote each other's neurotoxicity. Cultured neurons were protected by PACAP27 from the neurotoxicity of H2O2 but not through the activation of PACAP-27 receptor.
