Abstract
The aim of this study was to investigate the cellular and molecular mechanisms of declined intestinal transit (IT) function in the cholesterol gallstone (CG) formation process. Forty guinea pigs were divided into an experimental group (EG) and a control group (CoG), and the reverse transcription-polymerase chain reaction (RT-PCR) was performed for the analysis of c-kit and stem cell factor (scf) mRNA expression in the small bowel. In addition, immunofluorescence staining and confocal laser microscopy were performed for the observation of the changes in the number of interstitial cells of Cajal (ICCs) in the terminal ileum of each group. RT-PCR showed that, compared with the CoG, the intestinal c-kit and scf mRNA expression levels in the EG were significantly decreased; the average positive area of ICCs in the ileum in the EG was also significantly reduced. During the diet-induced CG formation procedure, the c-kit and scf mRNA expression levels in the small intestine decreased and the number of ICCs decreased. Inhibition of the c-kit/scf pathway may be involved in the declined IT function during the CG formation process.
Highlights
Introduction declinedintestinal transit (IT) may play an important role in the process of cholesterol gallstone (CG) formation.It has been demonstrated that the interstitial cells of Cajal (ICCs) are the pacemaker cells of the gastrointestinal slow wave, regulating the pacing and spreading of smooth muscle activity and participating in the conduction of nerve signal pathways [4,5,6]
There were no cases of mortality in the control group (CoG), and the guinea pigs grew in good condition
At the end of the lithogenic period, the dissection revealed that the gallbladders of the experimental group (EG) guinea pigs were swollen, with evident granular, yellow, single or multiple stones
Summary
Introduction declinedIT may play an important role in the process of CG formation.It has been demonstrated that the interstitial cells of Cajal (ICCs) are the pacemaker cells of the gastrointestinal slow wave, regulating the pacing and spreading of smooth muscle activity and participating in the conduction of nerve signal pathways [4,5,6]. The signaling pathway resulting from the combination of c‐kit and its ligand stem cell factor (scf) plays an important role in the development, differentiation and phenotypic maintenance of ICCs [7,8]. Whether the declined IT in the high‐cholesterol diet‐induced guinea pig CG model is caused by abnormalities in the ICCs and c‐kit/scf pathway remains to be investigated. In this experiment, immunofluorescence staining and the reverse transcription‐polymerase chain reaction (RT‐PCR) were performed to detect the number of ICCs in guinea pig small intestine tissue and to analyze the mRNA expression of c‐kit and scf, respectively. The aim of the study was to explore the cellular and molecular mechanisms of the IT decline during the CG formation process of the guinea pig
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