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DOI: 10.1055/s-0029-1186197
© Georg Thieme Verlag KG Stuttgart · New York
Luteolin Inhibits Lysophosphatidylcholine-Induced Apoptosis in Endothelial Cells by a Calcium/Mithocondrion/Caspases-Dependent Pathway
Publication History
received July 16, 2009
revised Sept. 14, 2009
accepted Sept. 16, 2009
Publication Date:
14 October 2009 (online)
Abstract
Luteolin, a naturally occurring polyphenol flavonoid, has demonstrated some beneficial modulation toward the endothelium. This study aims to investigate the effects of luteolin on lysophosphatidylcholine (LPC)-induced apoptosis, a key event in the pathogenesis of atherosclerosis, in endothelial cells. Luteolin reduced not only LPC-induced cell death but also lactate dehydrogenase (LDH) leakage. Luteolin inhibition of LPC-induced apoptosis in endothelial cells demonstrated its protection against the cytotoxicity of LPC. LPC-induced apoptosis is characterized by a calcium-dependent mitochondrial pathway, involving calcium influx, activation of calpains, cytochrome C release and caspases activation. Luteolin reduced calcium influx. It also inhibited calpains activation and prevented the release of cytochrome C from mitochondrion. The inhibition of cytochrome C release by luteolin blocked the activation of caspase-3 and thus prevented subsequent endothelial cell apoptosis. These results suggested that luteolin inhibits LPC-induced apoptosis in endothelial cells through the blockage of the calcium-dependent mitochondrial pathway.
Key words
luteolin - lysophosphatidylcholine - apoptosis - endothelial cells
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Prof. Dr. Baolin Liu
Department of Pharmacology of Chinese Materia Medica
China Pharmaceutical University
639 Longmian Road
210198 Nanjing
P. R. China
Phone: + 86 0 25 85 32 20 09
Fax: + 86 0 25 85 39 12 39
Email: submission2009@yahoo.cn