Emodin inhibits TNF-alpha-induced human aortic smooth-muscle cell proliferation via caspase- and mitochondrial-dependent apoptosis.

Abstract:

:Vascular smooth-muscle cell (VSMC) proliferation plays a vital role in hypertension, atherosclerosis and restenosis. It has been reported that emodin, an active component extracted from rhubarb, can stop the growth of cancer cells; however, it is not known if emodin exerts similar anti-atherogenic effects in TNF-alpha treated human aortic smooth-muscle cells (HASMC). In this study, emodin treatment showed potent inhibitory effects in TNF-alpha-induced HASMC proliferation that were associated with induced apoptosis, including the cleavage of poly ADP-ribose polymerase (PARP). Moreover, inhibitors of caspase-3, -8 and -9 (Ac-DEVD-CHO, Z-IETD-FMK and Z-LEHD-FMK) efficiently blocked emodin-induced apoptosis in TNF-alpha treated HASMC. Therefore, emodin-induced cell death occurred via caspase-dependent apoptosis. Emodin treatment resulted in the release of cytochrome c into cytosol and a loss of mitochondrial membrane potential (DeltaPsi(m)), as well as a decrease in the expression of an anti-apoptotic protein (Bcl-2) and an increase in the expression of an a pro-apoptotic protein (Bax). Emodin-mediated apoptosis was also blocked by a mitochondrial membrane depolarization inhibitor, which indicates that emodin-induced apoptosis occurred via a mitochondrial pathway. Taken together, the results of this study showed that emodin inhibits TNF-alpha-induced HASMC proliferation via caspase- and a mitochondrial-dependent apoptotic pathway. In addition, these results indicate that emodin has potential as an anti-atherosclerosis agent.

journal_name

J Cell Biochem

authors

Heo SK,Yun HJ,Park WH,Park SD

doi

10.1002/jcb.21805

subject

Has Abstract

pub_date

2008-09-01 00:00:00

pages

70-80

issue

1

eissn

0730-2312

issn

1097-4644

journal_volume

105

pub_type

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