Effect of danshensu on activation of JNK pathway in hepatic stellate cells(HSCs) induced by IL-1 beta.
- Author:
Bin-bin YU
1
;
Li-li DAI
;
Xin LI
;
Dong LI
;
Zhong-hua JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blotting, Western; Cell Proliferation; drug effects; Cells, Cultured; Collagen Type I; metabolism; secretion; Dose-Response Relationship, Drug; Down-Regulation; Hepatic Stellate Cells; drug effects; metabolism; Immunohistochemistry; Interleukin-1beta; pharmacology; JNK Mitogen-Activated Protein Kinases; metabolism; Lactates; administration & dosage; pharmacology; Liver Cirrhosis; etiology; prevention & control; Male; Mitogen-Activated Protein Kinases; metabolism; Rats; Rats, Wistar; Signal Transduction; drug effects
- From: Chinese Journal of Hepatology 2009;17(6):451-454
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo investigate the inhibitory effect of danshensu on the activation of JNK signaling in rat hepatic stellate cells (HSCs) induced by IL-1beta.
METHODSThe proliferation of primary rat HSCs treated with different concentration of Danshensu was checked by MTT colorimetric assay. The expression and phosphorylation of JNK and P-JNK was detected by western blotting. Synthesis and secretion of collagen I were detected by the quantitative immunocytochemical assay and ELISA.
RESULTSDanshensu inhibited the proliferation of HSCs in a dose-dependent manner. At the concentration of 0.0625 to 0.25 mmol/L, Danshensu significantly repressed the proliferation of HSC induced by IL-1beta (P < 0.05). Synthesis and secretion of Type I collagen was significantly decreased 24 hours after 0.25 mmol/L Danshensu treatment (P < 0.01). The phosphorylation of JNK induced by IL-1beta was significantly inhibited by Danshensu treatment (P < 0.05), however, the expression of JNK was not regulated by Danshensu.
CONCLUSIONDanshensu represses the activation and proliferation of HSCs, and inhibits the synthesis and secretion of Type I collagen, possibly via the repression of the JNK signal transduction.
