Aminoguanidine suppresses methylglyoxal-mediated oxygen-glucose deprivation injury in human brain microvascular endothelial cells.
- Author:
Wenlu LI
1
;
Quan HU
;
Xia REN
;
Ping HE
;
Huimin XU
;
Haibin DAI
;
Zhong CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Hypoxia; drug effects; Cell Survival; drug effects; Cells, Cultured; Drug Antagonism; Endothelial Cells; drug effects; metabolism; pathology; Endothelium, Vascular; cytology; Glycation End Products, Advanced; metabolism; Guanidines; pharmacology; Humans; Pyruvaldehyde; pharmacology
- From: Journal of Zhejiang University. Medical sciences 2013;42(3):261-266
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the effects of aminoguanidine on methylglyoxal-mediated oxygen-glucose deprivation (OGD) injury in the cultured human brain microvascular endothelial cells (HBMEC).
METHODSCultured HBMEC cells were pretreated with methylglyoxal before oxygen-glucose deprivation injury. Cell vitality was determined by MTT method, cell mortality was assessed by LDH release method, cell apoptosis was examined by Annexin V/PI formation method, and the advanced glycation end products (AGEs) were detected by Western-blot.
RESULTSMethylglyoxal induced HBMEC injury in a dose-dependent manner. At 2 mmol/L of methylglyoxal, the cell viability was 56.1% when methylglyoxal-pretreated cells exposed to oxygen-glucose deprivation, the cell inhibition rate was 90.0%. Aminoguanidine (1 mmol/L) inhibited methylglyoxal and OGD induced LDH release and Annexin V/PI formation. Furthermore, aminoguanidine (1 mmol/L) also decreased advanced glycation end products (AGEs) formation induced by methylglyoxal and oxygen-glucose deprivation.
CONCLUSIONAminoguanidine protected methylglyoxal mediated-oxygen-glucose deprivation injury in the cultured HBMEC, which may be associated with anti-glycation activity.