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Updated: Dec 24, 2025

Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Ribonuclease attenuates acute intestinal injury induced by intestinal ischemia reperfusion in mice
Xi-Yang Zhang1, Hai-Su Liang2, Jing-Juan Hu1
1Department of Anesthesiology, Nan Fang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Abstract:
Ribonuclease (RNase) reportedly exerts organ-protective effects in several pathological conditions, including ischemia reperfusion (I/R), but whether it can exhibit protective effect on intestinal I/R injury and potential mechanisms remain unknown. The present study was aimed to evaluate the effects of RNase on intestinal I/R injury and explore the underlying mechanisms. Thirty-two wild-type C57BL/6J adult male mice were evenly divided into a sham group, a sham + RNase group, an I/R group and an I/R + RNase group. Intestinal I/R was produced by clamping the superior mesenteric artery for 1 h followed by reperfusion for 2 h. All mice were treated with 3 doses of RNase or the same dosage of normal saline at different points. It was found that intestinal I/R caused significant intestinal injury and an increase in levels of extracellular RNAs (exRNAs). Treatment with RNase significantly reduced the inflammatory cytokine production, inhibited intestinal apoptosis and down-regulated the expression of toll like receptor 3 in intestinal tissues. In conclusion, increased exRNAs may contribute to intestinal I/R injury in adult mice, and RNase treatment during perioperative window is effective for attenuating intestinal I/R injury.
Insights
Ribonuclease (RNase) treatment protects against intestinal ischemia reperfusion (I/R) injury by reducing inflammation and apoptosis. This study shows RNase is a potential therapeutic for I/R injury.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Ribonuclease (RNase) has demonstrated organ-protective properties in various conditions.
- The role of RNase in mitigating intestinal ischemia reperfusion (I/R) injury and its underlying mechanisms are not well understood.
Purpose of the Study:
- To investigate the protective effects of RNase on intestinal I/R injury in a mouse model.
- To explore the potential mechanisms by which RNase exerts its protective effects.
Main Methods:
- A mouse model of intestinal I/R was established by clamping the superior mesenteric artery.
- Mice were divided into sham, sham + RNase, I/R, and I/R + RNase groups.
- RNase or saline was administered at specific time points during the experiment.
Main Results:
- Intestinal I/R induced significant injury and increased extracellular RNA (exRNA) levels.
- RNase treatment markedly reduced inflammatory cytokine production.
- RNase administration inhibited intestinal apoptosis and downregulated toll-like receptor 3 expression.
Conclusions:
- Elevated exRNAs appear to contribute to intestinal I/R injury.
- Perioperative RNase treatment effectively attenuates intestinal I/R injury in mice.
- RNase represents a promising therapeutic strategy for intestinal I/R injury.
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