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Updated: Apr 6, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
The Protective Effects of Ramelteon on Acute Intestinal Injury Caused by Experimentally Induced Endoplasmic Reticulum
Atilla Topcu1, Aykut Ozturk2, Esra Deniz1
1Faculty of Medicine, Department of Pharmacology, Recep Tayyip Erdogan University, Rize, Turkey.
Introduction:
Intestinal circulatory disturbances have been shown to cause increase endoplasmic reticulum (ER) stress.
Methods:
Forty-eight male Sprague Dawley rats were divided into six groups. The control group received saline solution alone. In the mesenteric artery ischemia (MAI) group, the mesenteric artery was occluded, and intestinal ischemia was induced for 1 h, and then terminated. The MAI + Ramelteon (Ram) group received 10 mg/kg Ram for 7 d. The final dose of Ram was administered half an hour prior to exposure to MAI on day 7. The MAI and reperfusion (MAI/R) group underwent 1 h of ischemia followed by 1 h of induced ischemia-reperfusion injury, respectively. The MAI/R + Ram group received 10 mg/kg Ram for 7 d before reperfusion induction. The final dose of Ram on day 7 was applied in the second half hour following ischemia induction. The Sham + Ram 10 mg/kg group received Ram for 7 d. Malondialdehyde, glutathione, tumor necrosis factor alpha, interleukin-10, caspase-3, 8-hydroxy-2'-deoxyguanosine, CAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), and glucose-regulated protein 78 levels were then examined.
Results:
Oxidative stress and inflammation induced by MAI and MAI/R activated the ER stress cascade. Through its protective effects, Ram significantly attenuated the elevated CHOP expression levels observed (P = 0.003 for MAI + Ram compared to MAI and P = 0.001 for MAI/R + Ram compared to MAI/R). Conversely, a significant increase in levels of the anti-inflammatory cytokine interleukin-10 was detected (P < 0.05).
Conclusions:
Ram appears to possess the potential ability to ameliorate experimentally induced small bowel damage by suppressing ER stress.
Insights
Ramelteon (Ram) treatment significantly reduced endoplasmic reticulum (ER) stress markers in rats experiencing intestinal ischemia and reperfusion injury. This suggests Ramelteon may protect against experimentally induced small bowel damage.
Area of Science:
- Gastroenterology
- Cellular Biology
- Pharmacology
Background:
- Intestinal circulatory disturbances are linked to increased endoplasmic reticulum (ER) stress.
- ER stress plays a role in the pathophysiology of intestinal ischemia and reperfusion (I/R) injury.
Purpose of the Study:
- To investigate the potential protective effects of Ramelteon (Ram) against experimentally induced intestinal ischemia and reperfusion (I/R) injury.
- To determine if Ramelteon can attenuate ER stress markers in a rat model.
Main Methods:
- Male Sprague Dawley rats were subjected to mesenteric artery ischemia (MAI) or MAI with reperfusion (MAI/R).
- Ramelteon (10 mg/kg) was administered for 7 days prior to or during the injury protocol.
- Levels of oxidative stress, inflammation, and ER stress markers (e.g., CHOP, IL-10) were measured.
Main Results:
- Mesenteric artery ischemia and reperfusion induced significant oxidative stress, inflammation, and ER stress.
- Ramelteon treatment significantly attenuated the elevated expression of the ER stress marker CHOP in both MAI and MAI/R groups.
- Ramelteon administration led to a significant increase in the anti-inflammatory cytokine interleukin-10.
Conclusions:
- Ramelteon demonstrates potential therapeutic value in ameliorating experimentally induced small bowel damage.
- The protective effects of Ramelteon appear to be mediated, at least in part, by the suppression of endoplasmic reticulum stress.
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