ArticleWorld journal of gastroenterology2013
Involvement of interstitial cells of Cajal in experimental severe acute pancreatitis in rats.
Article in World journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02412826 (Abstats), which is not on this map. Cited by 5 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Abstats: Computer-aided, Non-invasive, Acoustic Gastrointestinal Surveillance (AGIS) in Acute Pancreatitis
Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- The mechanism of transcutaneous gastric pacing treatment on gastrointestinal motility recovery and inflammation improvement in early-stage acute pancreatitis patients.BMC gastroenterology · 2024Trial
- Protective Effects of Calcitonin Gene-Related Peptide-Mediated p38 Mitogen-Activated Protein Kinase Pathway on Severe Acute Pancreatitis in Rats.Digestive diseases and sciences · 2019Article
- Association between acute pancreatitis and small intestinal bacterial overgrowth assessed by hydrogen breath test.World journal of gastroenterology · 2017Observational
- miR-551b-5p increases intracellular CaInternational journal of clinical and experimental pathology · 2017Article
- Interstitial cells of Cajal: update on basic and clinical science.Current gastroenterology reports · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo observe the changes in interstitial cells of Cajal (ICC) in rats with experimental severe acute pancreatitis (SAP).
methodsA 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.
resultsThere 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.
conclusionDecreased 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.
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