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HERO ID
538113
Reference Type
Journal Article
Title
Salvia miltiorrhiza Bunge and its active component cryptotanshinone protects primary cultured rat hepatocytes from acute ethanol-induced cytotoxicity and fatty infiltration
Author(s)
Yin, HQ; Choi, YJ; Kim, YC; Sohn, DH; Ryu, SY; Lee, BH
Year
2009
Is Peer Reviewed?
Yes
Journal
Food and Chemical Toxicology
ISSN:
0278-6915
EISSN:
1873-6351
Volume
47
Issue
1
Page Numbers
98-103
Language
English
PMID
19013495
DOI
10.1016/j.fct.2008.10.018
Web of Science Id
WOS:000262775900014
Abstract
Alcoholic liver disease involves hepatocellular injury induced by the acute or chronic consumption of ethanol. Fatty infiltration is usually followed by inflammation and focal necrosis, which can lead to cirrhosis if not treated properly in the initial stage. There have been many attempts to develop effective therapies for the disease, using natural products derived from medicinal plants. In this study, we report that the standardized fraction of Salvia miltiorrhiza Bunge (Sm-SF) and its active component, cryptotanshinone, were able to protect hepatocytes from lipopolysaccharide- and ethanol-induced cell death. They also suppressed ethanol-induced lipid accumulation as evidenced by the Nile red binding assay. The ethanol-induced activation and nuclear translocation of sterol regulatory element-binding protein-1 and the consequent transactivation of the target genes involved in fatty acid biosynthesis were inhibited by Sm-SF and cryptotanshinone in a dose-dependent manner. Cryptotanshinone, an active component of S. miltiorrhiza, has the potential to ameliorate alcoholic liver disease by blocking hepatic cell death and fatty acid synthesis. (C) 2008 Elsevier Ltd. All rights reserved.
Keywords
Salvia miltiorrhiza; Cryptotanshionone; Primary rat hepatocytes; Alcoholic liver disease; Sterol regulatory element-binding protein-1; tumor-necrosis-factor; alcoholic liver-disease; nitric-oxide synthase; tnf-alpha production; gene-expression; tanshinone-iia; inflammatory; response; induced apoptosis; egr-1 expression; lipid-metabolism
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