Premium
Luteolin inhibits pyrogallol‐induced apoptosis through the extracellular signal‐regulated kinase signaling pathway
Author(s) -
He Dongxu,
Ma Xin,
Chen Yun,
Cai Yanfei,
Ru Xiaochen,
Bruce Iain C.,
Xia Qiang,
Shi Guiyang,
Jin Jian
Publication year - 2012
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2012.08558.x
Subject(s) - luteolin , apoptosis , chemistry , signal transduction , umbilical vein , microbiology and biotechnology , reactive oxygen species , p38 mitogen activated protein kinases , kinase , biochemistry , protein kinase a , biology , in vitro , antioxidant , quercetin
Luteolin is an antioxidative, antitumor and anti‐inflammatory flavone. It has been shown to reduce endothelial dysfunction, but the mechanism is not clear. We set out to explore the effects of luteolin on apoptosis and its mechanism of action in endothelial cells. The effect of luteolin on pyrogallol‐induced superoxide stress and the subsequent apoptosis was studied in the mouse heart capillary endothelial cell line H5V and human umbilical vein endothelial cells, by the use of flow cytometry, 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐tetrazolium bromide, Hoechst staining, and western blot. Pyrogallol (0–400 μ m ) dose‐dependently induced reactive oxygen species production, cytotoxicity, an annexin V–fluorescein isothiocyanate increase, mitochondrial transmembrane depolarization and DNA condensation in both H5V and human umbilical vein endothelial cells; these actions were reversed by luteolin (0.78–50 μ m ) in a concentration‐dependent manner. Luteolin suppressed the poly (ADP‐ribose) polymerase activation, caspase‐8 cleavage and p38 mitogen‐activated protein kinase activation triggered by pyrogallol, and stimulated the extracellular signal‐regulated kinase signaling pathway to counteract the pyrogallol‐induced apoptotic signals. Luteolin is an effective agent for the protection of endothelial cells from superoxide stress‐induced apoptosis via the extracellular signal‐regulated kinase signaling pathway.