Premium
Puerarin protects human umbilical vein endothelial cells against high glucose‐induced apoptosis by upregulating heme oxygenase‐1 and inhibiting calpain activation
Author(s) -
Chen YingYing,
Chen Jie,
Zhou XinMei,
Meng XiangHong,
Jiang JianPing,
Shen YueLiang
Publication year - 2012
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2011.00926.x
Subject(s) - puerarin , calpain , umbilical vein , apoptosis , chemistry , downregulation and upregulation , heme oxygenase , caspase 3 , human umbilical vein endothelial cell , microbiology and biotechnology , heme , biochemistry , biology , programmed cell death , medicine , enzyme , in vitro , pathology , alternative medicine , gene
The aim of this study was to investigate whether puerarin protects against high glucose (HG)‐induced apoptosis by suppressing calpain activation in human umbilical vein endothelial cells (HUVECs). HUVECs were exposed to normal glucose (NG) (5.5 m m ) or HG (33 m m ) for 48 h; then, apoptosis and caspase‐3 activity were determined. The expression of heme oxygenase‐1 (HO‐1) mRNA was evaluated by RT‐PCR analysis. The activation of calpain and HO activity were also assessed. Compared with the NG group, exposure of HUVECs to HG for 48 h resulted in significant increases in calpain and caspase‐3 activity as well as apoptosis, which were prevented by co‐incubation with puerarin (1–100 μ m ) in a concentration‐dependent manner. HO‐1 mRNA expression and HO activity were decreased in HUVECs treated with HG for 48 h. Compared with the group exposed to HG alone, co‐incubation of HUVECs with puerarin and HG induced increases in HO‐1 mRNA expression and HO activity. The HO‐1 inhibitor protoporphyrin IX zinc (II) abolished the inhibitory effect of puerarin on HG‐induced calpain and caspase‐3 activation, as well as apoptosis. The data show that puerarin protects against HG‐induced endothelial cell apoptosis by a mechanism involving upregulation of HO‐1 expression and inhibition of calpain activity.