The effect of rosiglitazone on the activity of STAT1 in rats with severe acute pancreatitis.
- Author:
Shun-Xin HAO
1
;
Wei-Xing WANG
;
Chen CHEN
;
Jia-Rui FENG
;
Heng YAN
Author Information
- Publication Type:Journal Article
- MeSH: Acute Disease; Animals; Disease Models, Animal; Male; Pancreas; metabolism; pathology; Pancreatitis; drug therapy; metabolism; pathology; Random Allocation; Rats; Rats, Wistar; STAT1 Transcription Factor; metabolism; Thiazolidinediones; pharmacology
- From: Chinese Journal of Surgery 2009;47(3):218-221
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of rosiglitazone on the activity of signal transducer and activator of transcription 1 in rats with severe acute pancreatitis.
METHODSFifty-four male Wistar rats were randomly allocated into three groups (n = 18). SO group: sham-operated animals served as control, operation was executed and sodium chloride but not sodium taurocholate was injected. SAP group: SAP was induced by the retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. ROSI group: same as SAP group, but rosiglitazone (6 mg/kg) was administered intravenously 30 min before operation. Rats in each group were sacrificed at 3,6 and 12 h after operation. The levels of serum amylase and histologic scores of pancreatic tissue were measured. The expression of TNF-alpha mRNA in pancreatic tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR). The expression of phosphorylated STAT1 in pancreatic tissue was assayed by immunohistochemistry.
RESULTSCompared to SO group, the levels of serum amylase and phosphorylated STAT1, TNF-alpha mRNA and histologic scores of pancreatic tissue were significantly elevated at the same time points after SAP (P < 0.01). The levels of these detection in ROSI group were lower than those of the SAP group at the same time points (P < 0.05), but higher than SO group (P < 0.05).
CONCLUSIONSSTAT1 was activated in severe acute pancreatitis. Rosiglitazone has a protective effects in rats with severe acute pancreatitis. The mechanism of its protective effects maybe that it inhibits the activation of JAK/STAT pathway, which can down-regulate the expression of TNF-alpha mRNA and block the the inflammatory cascade partially.