Objective:To investigate the effect of Modified Xiaochaihu Decoction(MXD,加味小柴胡汤)on collagen degradation in rats with chronic pancreatitis(CP).Methods:Rats were injected dibutyltin dichloride(DBTC,7 mg/kg of body weight)into the right caudal vein to induce CP model.Thirty heallhy male Wistar rats were randomly divided into three groups by a random number table:the control,the model and the treatment groups.Rats of treatment group were administered MXD(10 g/kg of body weight)orally once daily starting from the day post-model establishment.Pancreatic tissues were harvested after 28-day feeding and fibrosis was evaluated by picro-sirius red staining.The contents of collagen typeⅠandⅢwere detected using enzymelinked immunosorbent assay(ELISA),the expression of matrix metalloproteinase 13(MMP13)and tissue inhibitor of metalloproteinase 1(TIMP1)was analyzed by Western blot and real-time polymerase chain reaction(PCR).Results:The fibrosis scoring of pancreatic tissues,the concentrations of collagen typeⅠandⅢ,the expression levels of MMP13 and TIMP1 proteins and mRNA in the model group were all increased compared with the control group(P<0.05).After treatment with MXD,the fibrosis scoring of pancreatic tissues,the concentrations of collagen typeⅠandⅢ,the expression levels of MMP13 proteins and m RNA in the teatment group were all decreased compared with the model group(P<0.05),but there were no significant differences in the expression levels of TIMP1 proteins and m RNA(P>0.05).Conclusion:MXD could promote collagen degradation and reverse pancreatic fibrosis in CP rats via a mechanism involve up-regulation of MMP13 expression.
Objective： To investigate the effect of modified Xiaochaihu Decoction （小柴胡汤, MXD） on transforming growth factor- [3 1/Sma- and Mad-related proteins （TGF- 13 1/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- β 1, TGF- β 1 type Ⅱ receptor （TGF β R 11 ）, 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- β 1, TGF β R 11 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-β 1/Smads signaling pathway.
