Effects of rosiglitazone on Kruppul-like factor 6 (KLF6) signaling in the livers of rats with nonalcoholic fatty liver fibrosis.
- Author:
Xiao-min WANG
1
;
Dong-feng CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Fatty Liver; metabolism; pathology; Kruppel-Like Factor 6; Kruppel-Like Transcription Factors; metabolism; Liver; metabolism; Male; PPAR gamma; metabolism; Proto-Oncogene Proteins; metabolism; Rats; Rats, Wistar; Signal Transduction; drug effects; Thiazolidinediones; pharmacology; Transforming Growth Factor beta1; metabolism
- From: Chinese Journal of Hepatology 2007;15(9):649-653
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of rosiglitazone on Kruppule-like factor 6 (KLF6) and its target gene TGFâ1 during the development of nonalcoholic fatty liver fibrosis.
METHODThirty-six Wistar rats were divided into three groups: a control group, a high fat model group and an intervention group. Their blood serum TG, FFA, AST, ALT, HA, LN and CIV were measured. Hepatic expressions of KLF6, TGFbeta1 and alpha-SMA were detected by RT-PCR and immunohistochemistry. The pathological features and the degree of liver fibrosis before and after the rosiglitazone intervention were also studied.
RESULTSThe contents of TG, FFA, AST, ALT, HA, LN and CIV, the expression of KLF6, TGFbeta1 and alpha-SMA mRNA, and the degree (score) of liver fibrosis at the 24th week in the model group were significantly higher than those in the control group (P<0.01) but they were lower in the rosiglitazone intervention group (P<0.05). The protein expression of a-SMA was also lower in the intervention group compared with that of the model group.
CONCLUSIONRosiglitazone, to a certain extent, can inhibit KLF6-TGFbeta1 signal transduction by inducing expression of PPAR-gamma, and then inhibit the activation of hepatic stellate cells and minimize hepatic fibrosis.
