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Cytoprotective effect of a synthetic triterpenoid against oxidative stress in human umbilical vein endothelial cells (HUVEC)
Author(s) -
Wang Xinyu Eric,
Stavchansky Salomon,
Bowman Phillip
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.937.7
Subject(s) - caffeic acid phenethyl ester , oxidative stress , menadione , umbilical vein , chemistry , heme oxygenase , pharmacology , cytoprotection , biochemistry , heme , microbiology and biotechnology , enzyme , biology , caffeic acid , antioxidant , in vitro
Induction of phase II enzymes, in particular the 32 kd stress protein heme oxygenase‐1 (HO‐1), is cytoprotective in human endothelial cells. We previously demonstrated that caffeic acid phenethyl ester (CAPE) was cytoprotective against menadione‐induced oxidative stress in HUVEC largely via the induction of HO‐1.* Here, we tested the cytoprotective activity of 1[2‐cyano‐3,12‐dioxooleana‐1,9(11)‐dien‐28‐oyl]imidazole (CDDO‐Im), a new synthetic triterpenoid (Dr. Michael Sporn, Dartmouth University) against oxidative stress. Dose response studies indicated that CDDO‐Im at 100 nM was more cytoprotective against menadione toxicity than an optimal dose of CAPE (20 µM), resulting in endothelial cell survival of 80% compared to 60% for CAPE. Messenger RNA for HO‐1 was increased 90‐fold in the presence of CDDO‐Im, while only 13‐fold by CAPE. Western blot analysis of HO‐1 protein product indicated that by 6 h, CDDO‐Im induced an 8‐fold higher level of HO‐1 while CAPE induced a 2‐fold increase. The results indicate that CDDO‐Im is a much more potent cytoprotectant than CAPE, and this beneficial effect correlates well with the induction of HO‐1. *Wang X, et al. Eur J Pharmacol. 2008 Sep 4;591(1‐3):28‐35.