Published online Apr 28, 2014. doi: 10.3748/wjg.v20.i16.4712
Revised: January 20, 2014
Accepted: March 4, 2014
Published online: April 28, 2014
Processing time: 173 Days and 20.1 Hours
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.
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.