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Grape seed procyanidin B2 inhibits advanced glycation end product‐induced endothelial cell apoptosis through regulating GSK3β phosphorylation
Author(s) -
Li Baoying,
Li Xiaoli,
Gao Haiqing,
Zhang Jianhua,
Cai Qian,
Cheng Mei,
Lu Mei
Publication year - 2011
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100656
Subject(s) - glycation , phosphorylation , apoptosis , microbiology and biotechnology , advanced glycation end product , chemistry , gsk 3 , biology , biochemistry , receptor
To investigate the effects of GSPB2 (grape seed procyanidin B2) on the apoptosis of HUVECs (human umbilical endothelial cells) induced by AGEs (advanced glycation end products), HUVECs were treated with AGEs (200 μg/ml) in the presence or absence of GSPB2 (2.5, 5.0 and 10.0 μmol/l). Our findings showed that (i) AGEs induced HUVEC apoptosis and up‐regulated the expression of caspase‐3 activation and lactadherin and reduced the phosphorylation of GSK3β (glycogen synthase kinase 3β) at baseline. (ii) Treatment of HUVEC with GSPB2 significantly inhibited the cell apoptosis and the expression of caspase‐3 activation and lactadherin induced by AGEs. Moreover, GSPB2 inhibited intracellular reactive oxygen species in a dose‐dependent manner in AGEs‐treated cells as determined by flow cytometry. (iii) GSPB2 increased the phosphorylation of GSK3β of HUVEC in response to AGEs. These findings suggest that the signalling pathway involving phosphorylation of GSK3β and lactadherin might play a key role in the endothelial apoptosis. GSPB2 therapy could become an effective approach to battling AGEs‐induced endothelial apoptosis.