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Ganoderma lucidum extract attenuates the proliferation of hepatic stellate cells by blocking the PDGF receptor
Author(s) -
Wang GueiJane,
Huang YehJeng,
Chen DengHai,
Lin YunLian
Publication year - 2009
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2687
Subject(s) - hepatic stellate cell , ganoderma lucidum , platelet derived growth factor receptor , blocking (statistics) , traditional medicine , receptor , pharmacology , platelet derived growth factor , chemistry , biology , medicine , growth factor , computer science , computer network
Hepatic fibrosis is an outcome of chronic liver diseases. The activation and proliferation of hepatic stellate cells (HSCs) is a key event in liver injury. The fruiting body of Ganoderma lucidum has long been a popular oriental medicine for treating liver diseases. The aim of this present study was to investigate the antiproliferative effects of the triterpenoid‐rich extract (GLT) of G. lucidum in a cell line of rat HSCs (HSC‐T6) stimulated with platelet‐derived growth factor (PDGF)‐BB. DNA synthesis was investigated by bromodeoxyuridine (BrdU) incorporation. Flow cytometry using propidium iodide (PI) labeling was carried out to analyse the cell cycle distribution and apoptosis. α ‐Smooth muscle actin ( α ‐SMA) was used to evaluate extracellular matrix deposition, and western blotting was performed to measure cyclins D1 and D2, and phosphorylation of the PDGF β ‐receptor (PDGF β R), Akt and JNK. The results indicated that the GLT attenuated BrdU incorporation in a concentration‐dependent manner with an IC 50 of 8.52 ± 0.33 µg/mL. The inhibitory effect of the GLT was associated with downregulation of cyclins D1 and D2, and PDGF β R and Akt phosphorylation, upregulation of JNK phosphorylation, and a reduction in α ‐SMA expression. These results indicated that G. lucidum inhibits PDGF‐BB‐activated HSC proliferation possibly through blocking PDGF β R phosphorylation, thereby indicating its efficacy for preventing and treating hepatic fibrosis. Copyright © 2008 John Wiley & Sons, Ltd.