Effect of genistein on MAPK signal pathway in the collagen-induced arthritis fibroblast-like synoviocytes.
- Author:
Xue-zeng ZHANG
1
;
Yu ZHANG
;
Wei-gan SHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Arthritis, Experimental; metabolism; Cells, Cultured; Extracellular Signal-Regulated MAP Kinases; metabolism; Female; Genistein; pharmacology; MAP Kinase Signaling System; drug effects; Rats; Rats, Sprague-Dawley; Synovial Membrane; cytology; drug effects; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2011;31(10):1405-1408
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of genistein (Gen) on MAPK signal pathway in the CIA rat fibroblast-like synoviocytes (FLS).
METHODSThe rat model of collagen-induced arthritis (CIA) was established. The cultured FLS of CIA rats were divided using randomized method. The effects of Gen (at the concentration of 50, 100, and 200 micromol/L, respectively) on the proliferation of FLS in CIA rats using methyl thiazolyl tetrazolium (MTT) assay. Effects of Gen (at the concentration of 50, 100, and 200 pmol/L, respectively) on the expressions of extracellular signal-regulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) in the FLS of CIA rats were detected.
RESULTSGen could inhibit the proliferation of FLS in CIA rats. The FLS proliferation in the high dose Gen group at 72 h was only 1.10+/-0.04, significantly lower than that in the model group (2.12+/-0.03, P<0.01). Besides, after Gen's action on FLS, the expression of p-ERK was down-regulated. It was only 0.34+/-0.02 in the high dose Gen group, significantly lower than that in the model group (2.68+/-0.14, P<0.01). There was no change in the expression of ERK (P>0.05).
CONCLUSIONSGen could inhibit the proliferation of FLS in CIA rats. Its mechanism of action was mainly correlated to down-regulating the tyrosine kinase of MAPK signal transduction pathway and inhibiting phosphorylation of ERK.
