Digestive diseases and sciences · 2010
Pioglitazone: a promising therapeutic tool in sodium taurocholate-induced severe acute pancreatitis.
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Xu Ping, Xu Kai, Wang Jing, Jiang Jin-Ping, Chen Ling-Quan
Аннотация
BACKGROUND: Studies suggest that peroxisome proliferator-activated receptor γ(PPARγ) ligands may represent a therapeutic option in acute pancreatitis, yet most of them have been prophylactic administrated.
AIMS: To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate.
METHODS: Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined.
RESULTS: Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved.
CONCLUSIONS: Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.
AIMS: To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate.
METHODS: Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined.
RESULTS: Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved.
CONCLUSIONS: Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.