Imeglimin confers protection against intestinal ischemia/reperfusion injury in rats through AMPK-dependent inhibition of NF-κB/NLRP3 inflammasome signaling and mitigation of oxidative stress and apoptosis.

Authors

Walaa Yehia Abdelzaher, Hanaa Mohamed Khalaf, Rabeh Khairy Saleh, Nehal Refaat Raouf, Youssra Magdy Hassan, Maggi Mofeed Ayad, Rania Rady Fadl

Published in

Inflammopharmacology. Jul 24, 2026. Epub Jul 24, 2026.

Abstract

Intestinal ischemia/reperfusion (I/R) injury is a critical condition characterized by oxidative stress, inflammation, and apoptosis, leading to significant tissue damage. Imeglimin (IMEG), a novel antidiabetic agent, has recently shown cytoprotective effects through modulation of mitochondrial function, oxidative stress, and inflammatory pathways. We aimed to investigate the potential protective effects of IMEG against II/R injury and to explore the underlying mechanisms involved.
Thirty-two adult male Wistar albino rats were divided into four groups; sham group, IMEG group, intestinal I/R group, IMEG + Intestinal I/R group. Oxidative stress markers [malondialdehyde (MDA), reduced glutathione (GSH)], and histopathological changes were assessed. Biochemical analyses included measurement of phosphorylated AMP-activated protein kinase (p-AMPK), NOD-like receptor protein 3 (NLRP3) and caspase-3. Also, gene expression of interleukin (IL)-1β, caspase-1, apoptotic Bcl-2-associated protein x (BAX) and anti-apoptotic B-cell leukemia/lymphoma 2 protein (Bcl-2) were measured. Nuclear factor-κB (NF-κB) immuno expression was estimated.
MDA, NLRP3, caspase-3 levels, IL-1β, caspase-1, Bax gene expression, and NF-κB immunohistochemical expression were all significantly elevated in the intestinal I/R group while GSH, p-AMPK levels and Bcl-2 gene expression were significantly decreased. Every metric indicated a notable improvement with IMEG.
IMEG exerts a protective effect against intestinal I/R injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties (Fig. 1).

PMID:
42498903
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.

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