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Expression of S mad7 and S mad ubiquitin regulatory factor 2 in a rat model of chronic pancreatitis
Author(s) -
Hou Xiao Jia,
Jin Zhen Dong,
Jiang Fei,
Zhu Jian Wei,
Li Zhao Shen
Publication year - 2015
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/1751-2980.12253
Subject(s) - medicine , ubiquitin , pancreatitis , cancer research , microbiology and biotechnology , gene , genetics , biology
Objective To quantify the expressions of S mad7 and S mad ubiquitin regulatory factor 2 ( S murf2) in the pancreas in rats with chronic pancreatitis ( CP ). Methods A total of 16 male Wistar rats were randomly divided into the control group and the CP group, with 8 rats in each group. CP was induced in vivo with dibutyltin dichloride ( DBTC ). Four weeks after DBTC administration, histological assessment and the measurement of hydroxyproline content in the pancreatic tissues were performed to assess the inflammation and fibrosis of the pancreas. Immunohistochemisty and reverse transcription polymerase chain reaction ( RT‐PCR ) for transforming growth factor ( TGF )‐β1 and α‐smooth muscle actin (α‐ SMA ) were applied to assess activated pancreatic stellate cells ( PSC ) and TGF ‐β1 expression. S mad7 and S murf2 expressions in the pancreas were measured using Western blot and RT‐PCR . Results Typical histopathological characteristics of DBTC ‐induced CP in the rats with extensively activated PSC . Compared with the control group, the expressions of TGF ‐β1 , α‐ SMA and hydroxyproline content in the pancreatic tissues in the CP group were significantly increased. Meanwhile, the m RNA and protein expressions of S mad7 and S murf2 were significant increased in the fibrotic pancreas, in which the expressions of S mad7 proteins showed an obvious reduction compared with controls. Conclusion The dysregulation of S mad7 and S murf2 may be associated with the pathogenesis of pancreatic fibrosis through the TGF ‐β signaling pathway.