Study on effects of extracts from Salvia Miltiorrhiza and Curcuma Longa in inhibiting phosphorylated extracellular signal regulated kinase expression in rat's hepatic stellate cells.
- Author:
Yang CHENG
1
;
Jian PING
;
Cheng LIU
;
Ying-zi TAN
;
Gao-feng CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Division; drug effects; Cell Line; Curcuma; Drugs, Chinese Herbal; pharmacology; Extracellular Matrix; drug effects; Extracellular Signal-Regulated MAP Kinases; metabolism; Hepatocytes; drug effects; enzymology; Liver Cirrhosis; drug therapy; metabolism; MAP Kinase Signaling System; drug effects; Phosphorylation; drug effects; Plant Extracts; Rats; Salvia miltiorrhiza; Vasodilator Agents; pharmacology
- From: Chinese journal of integrative medicine 2006;12(3):207-211
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the effect of salvianolic acid B (SAB) and curcumin, the extracts of Salvia Miltiorrhiza and Curcuma Longa, on the proliferation and activation of hepatic stellate cell (HSC), and the extracellular signal regulated kinase (ERK) expression in it.
METHODSRat's HSC-T6 were cultured and treated by SAB or curcumin. The inhibitory effect on cell proliferation was determined by 3-(4, 5-dimthyl-2-2thiazoly)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and the expression levels of alpha smooth actin (alpha-SMA), collagen type I, and ERK were determined by Western blot.
RESULTSSAB and curcumin inhibited the proliferation and activation of rat's HSC-T6 in dose-dependent fashion and significantly reduced the expression level of alpha-SMA (P < 0.01). Curcumin significantly reduced the expression of collagen type I (P < 0.05). Both SAB and curcumin showed insignificant effect on the ERK expression level, but they could significantly reduce the level of phosphorylated-ERK expression, showing significant difference as compared with that in the control group (P < 0.01 and P < 0.05 respectively).
CONCLUSIONSAB and curcumin could significantly inhibit the proliferation, activation of HSC, and the production of type I collagen in HSC, the mechanism may be associated with their inhibition on ERK phosphorylation.
