November 12, 2014
Notes: Shen, Jiaqing
Research Support, Non-U.S. Gov’t
Cytokine. 2013 Oct;64(1):382-94. doi: 10.1016/j.cyto.2013.05.012. Epub 2013 Jun 29.
Author Address: Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Jiangsu, China.
Reference Type: Journal Article
Record Number: 5316Author: Shi, L. L., Liu, M. D., Chen, M. and Zou, X. P.
Title: Involvement of interstitial cells of Cajal in experimental severe acute pancreatitis in rats
Journal: World J Gastroenterol
Short Title: Involvement of interstitial cells of Cajal in experimental severe acute pancreatitis in rats
Alternate Journal: World journal of gastroenterology : WJG
ISSN: 2219-2840 (Electronic)
Accession Number: 23599644
Keywords: Acute Disease
Disease Models, Animal
Interstitial Cells of Cajal/metabolism/*ultrastructure
Proto-Oncogene Proteins c-kit/genetics/metabolism
Severity of Illness Index
Abstract: AIM: To observe the changes in interstitial cells of Cajal (ICC) in rats with experimental severe acute pancreatitis (SAP). METHODS: A total of twenty-four SD rats were randomly divided into two groups (n = 12), namely the sham (S) group and the SAP group; the SAP rat model was established by retrograde injection of 5% sodium taurocholate (1.0 mL/kg) into the pancreatic duct. Twenty-four hours later intestinal motility was assessed by testing small intestinal propulsion rate, and then the rats were sacrificed. The pancreas and jejunum were resected and underwent routine pathologic examination. Immunohistochemical staining was used to detect c-kit-positive cells in the jejunum. Expression of c-kit mRNA was detected by real-time polymerase chain reaction, and the expression of c-kit protein was evaluated by Western blotting. Ultrastructure of ICC was evaluated by transmission electron microscopy. RESULTS: There was bleeding, necrosis and a large amount of inflammatory cell infiltration in pancreatic tissue in the SAP group, while in jejunal tissue we observed a markedly denuded mucosal layer, loss of villous tissue and a slightly dilated muscular layer. The small intestinal propulsion rate was 68.66% +/- 2.66% in the S group and 41.55% +/- 3.85% in the SAP group. Compared with the S group, the rate of the SAP group decreased sharply. The density of c-kit-positive cells in the SAP group was significantly lower than in the S group; the respective mean densities were 88.47 +/- 10.49 in the S group and 56.11 +/- 7.09 in the SAP group. The levels of c-kit protein and mRNA were 0.36 +/- 0.04 and 1.29 +/- 0.91 in the SAP group, respectively, which were significantly lower than those in the S group (0.53 +/- 0.06, 0.64 +/- 0.33, respectively). In the SAP group, ICC profiles showed the same change tendency, such as vacuolation of mitochondria, irregular vacuoles and loosened desmosome-like junctions. CONCLUSION: Decreased c-kit-positive cells and ultrastructural changes in ICC resulting from blockade of the c-kit signaling pathway are involved in the intestinal dysmotility associated with SAP.