Brief Article
Copyright ©2014 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Apr 28, 2014; 20(16): 4712-4717
Published online Apr 28, 2014. doi: 10.3748/wjg.v20.i16.4712
Sonic hedgehog expression in a rat model of chronic pancreatitis
Luo-Wei Wang, Han Lin, Yi Lu, Wei Xia, Jun Gao, Zhao-Shen Li
Luo-Wei Wang, Han Lin, Wei Xia, Jun Gao, Zhao-Shen Li, Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
Yi Lu, Department of Respiratory Medicine, Shanghai Sixth People’s Hospital, Shanghai Jiaotong University, Shanghai 200233, China
Author contributions: Wang LW and Lin H contributed equally to this work; Wang LW and Li ZS designed the research; Lin H, Lu Y, Xia W and Gao J performed the research; Wang LW and Xia W analyzed the data; Wang LW and Lin H wrote the paper.
Supported by National Natural Science Foundation of China, No. 30700360
Correspondence to: Zhao-Shen Li, MD, PhD, Professor, Department of Gastroenterology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China. zhsli@81890.net
Telephone: +86-21-25070552 Fax: +86-21-55621735
Received: November 6, 2013
Revised: January 20, 2014
Accepted: March 4, 2014
Published online: April 28, 2014
Abstract

AIM: To analyze the activation of sonic hedgehog (SHh) signaling pathways in a rat model of chronic pancreatitis.

METHODS: Forty Wistar rats were randomly divided into 2 groups: experimental group and control group (20 rats in each group). Dibutyltin dichloride was infused into the tail vein of the rats to induce chronic pancreatitis in the experimental group. The same volume of ethanol and glycerol mixture was infused in the control group. The expression of Ptch, Smo and Gli were analyzed using immunohistochemistry, and real-time reverse transcription polymerase chain reaction (RT-PCR).

RESULTS: Compared with the control group, significant histological changes in terms of the areas of abnormal architecture, glandular atrophy, fibrosis, pseudo tubular complexes, and edema were observed at week 4 in the experimental group. The expression of Ptch1, Smo and Gli1 in the pancreatic tissue increased significantly in the experimental group. Using RT-PCR, mRNA levels of Ptch, Smo and Gli in the experimental group increased significantly compared with the control group.

CONCLUSION: The SHh signaling pathway is aberrantly activated in rats with chronic pancreatitis. The SHh signaling pathway plays an important role in the development of chronic pancreatitis. These results may be helpful in studies focusing on the relationship between chronic pancreatitis and pancreatic cancer.

Keywords: Sonic hedgehog, Chronic pancreatitis, Pancreatic cancer, Ptch1, Smo, Gli1

Core tip: Chronic pancreatitis (CP) is a progressive inflammation of the pancreas in which pancreatic secretory parenchyma is destroyed and replaced by fibrous tissue, eventually leading to impairment of both exocrine and endocrine functions. Hedgehog (Hh) signaling is a developmental signaling pathway that is highly activated in the embryo and in the early postnatal phase. Studies on the Hh signaling pathway in human CP are restricted by limited availability of tissues. Therefore, the present study was carried out to analyze the activation of SHh signaling pathways in a rat model of CP.