Impact of acute stress on gastric interstitial cells of Cajal disorder.

INTRODUCTION

Acute stress can disrupt gastrointestinal function. Interstitial cells of Cajal (ICCs) regulate gastric motility; however, the effects underlying their alterations during stress remain unclear. We aimed to explore the potential impact of acute stress on alterations in gastric ICCs.

METHODS

Animals were assigned to one control and four study groups (0, 24, and 72 h). Acute stress was induced via right chest puncture using a Hopkinson bar. Lung injury was assessed using hematoxylin-eosin staining, gastric ICCs were examined using immunohistochemistry, immunohistofluorescence, and TdT-mediated dUTP nick-end labeling assays. Transmission electron microscopy was used to evaluate ultrastructural changes. Western blotting and real-time polymerase chain reaction were used to analyze SCF/c-kit, protein 53 (p53), and the Wnt/β-catenin signaling pathways. Enzyme-linked immunosorbent assay was used to quantify nuclear factor kappa B (NF-κB) p65, interleukin (IL)-1β, IL-6, IL-9, IL-10, tumor necrosis factor-alpha (TNF-α), and cortisol. Spectrophotometry was used to determine the levels of reactive oxygen species (ROS) and malondialdehyde (MDA).

RESULTS

The lung tissue exhibited congestion, edema, and the destruction of the alveolar structure following puncture. The gastric ICCs tested positive for the surface markers CD117/c-kit and CD34. The population and apoptosis of the gastric ICCs were altered in the acute stress condition. Moreover, acute stress caused dysregulated SCF/c-kit, Wnt/β-catenin, p53 and NF-κB pathways. IL-1β, IL-6, IL-9, IL-10, TNF-α, and cortisol demonstrated altered expression levels, whereas ROS and MDA were upregulated in the acute stress condition.

CONCLUSION

Acute stress damages gastric ICCs through the Wnt/β-catenin, JAK/STAT, and NF-κB signaling pathways, as well as p53-and SCF/c-kit pathway-mediated abnormalities and oxidative stress, contributing to functional alterations in gastric ICCs.