Reversing effect of histamine on neurotoxicity induced by beta-amyloid1-42.
- Author:
Qiu-Li FU
1
;
Hai-Bin DAI
;
Yao SHEN
;
Zhong CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; chemically induced; metabolism; prevention & control; Amyloid beta-Peptides; toxicity; Animals; Benzothiazoles; pharmacology; Diphenhydramine; pharmacology; Dose-Response Relationship, Drug; Histamine; pharmacology; Histamine H2 Antagonists; pharmacology; Histamine H3 Antagonists; pharmacology; Imidazoles; pharmacology; Neuroprotective Agents; metabolism; pharmacology; PC12 Cells; Phenoxypropanolamines; pharmacology; Piperidines; pharmacology; Rats; Receptors, Histamine H2; metabolism; Receptors, Histamine H3; metabolism; Thiourea; analogs & derivatives; pharmacology
- From: Journal of Zhejiang University. Medical sciences 2007;36(2):146-149
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of histamine on the neurotoxicity induced by beta-amyloid(1-42)(Abeta42) in rat phaeochromocytoma (PC12) cells.
METHODSThe in vitro model of Alzheimer's disease was constructed with A beta42-treated PC12 cells. Cell morphology and MTT assay were used to evaluate the cell toxicity and histamine effects. The different histamine antagonists were applied to investigate the involvement of receptor subtypes.
RESULTThe neurotoxicity was induced by A beta42 in a concentration-dependent manner, which was reversed by histamine at concentration of 10(-7), 10(-6) mol/L. The effect was reversed by H(2) antagonist zolantidine and H(3)antagonist clobenpropit, but not by H(1) antagonist diphenhydramine.
CONCLUSIONHistamine reduces neurotoxicity induced by beta-amyloid(1-42), which may be mediated by H(2) and H(3)receptors.
