OBJECTIVE: To investigate the effect of modified Xiaochaihu Decoction (, MXD) on transforming growth factor-β1/Sma- and Mad-related proteins (TGF-β1/Smads) signaling pathway in rats with chronic pancreatitis (CP) induced by dibutyltin dichloride. METHODS: Thirty healthy male Wistar rats were randomly divided into the normal control group, CP group and CP+MXD-treated group. CP was induced by injection of dibutyltin dichloride (DBTC, 7 mg/kg of body weight) into the right caudal vein, and the control rats were treated with vehicle. MXD was given daily by gavage at a dose of 10 g/kg of body weight, starting from the day after CP induction. After 28-day treatment, the n-benzoyl-tyrosyl para-aminobenzoic acid (NBT-PABA) test was carried out to evaluate exocrine pancreatic function. Then, rats were sacrificed, and pancreatic tissues were harvested for histological evaluation. In addition, the mRNA expression of TGF-β1, TGF-β1 type II receptor (TGFβRII), Smad3 and Smad7 was determined in pancreatic tissues by using real-time polymerase chain reaction. RESULTS: Treatment of CP with MXD improved the PABA recovery, decreased the histological lesion, and reduced the mRNA expression of TGF-β1, TGFβRII and Smad3 (P<0.05). However, MXD had no effect on Smad7 mRNA level. CONCLUSIONS: MXD could protect the pancreas against chronic injury and improve pancreatic exocrine function in DBTC induced rat CP model. Its mechanism may involve inhibition of the TGF-β1/Smads signaling pathway.
OBJECTIVE: To investigate the effect of modified Xiaochaihu Decoction (, MXD) on transforming growth factor-β1/Sma- and Mad-related proteins (TGF-β1/Smads) signaling pathway in rats with chronic pancreatitis (CP) induced by dibutyltin dichloride. METHODS: Thirty healthy male Wistar rats were randomly divided into the normal control group, CP group and CP+MXD-treated group. CP was induced by injection of dibutyltin dichloride (DBTC, 7 mg/kg of body weight) into the right caudal vein, and the control rats were treated with vehicle. MXD was given daily by gavage at a dose of 10 g/kg of body weight, starting from the day after CP induction. After 28-day treatment, the n-benzoyl-tyrosyl para-aminobenzoic acid (NBT-PABA) test was carried out to evaluate exocrine pancreatic function. Then, rats were sacrificed, and pancreatic tissues were harvested for histological evaluation. In addition, the mRNA expression of TGF-β1, TGF-β1 type II receptor (TGFβRII), Smad3 and Smad7 was determined in pancreatic tissues by using real-time polymerase chain reaction. RESULTS: Treatment of CP with MXD improved the PABA recovery, decreased the histological lesion, and reduced the mRNA expression of TGF-β1, TGFβRII and Smad3 (P<0.05). However, MXD had no effect on Smad7 mRNA level. CONCLUSIONS: MXD could protect the pancreas against chronic injury and improve pancreatic exocrine function in DBTC induced rat CP model. Its mechanism may involve inhibition of the TGF-β1/Smads signaling pathway.
Authors: H F Zhao; T Ito; J Gibo; K Kawabe; T Oono; T Kaku; Y Arita; Q W Zhao; M Usui; K Egashira; H Nawata Journal: Gut Date: 2005-12 Impact factor: 23.059