ArticleJournal of inflammation (London, England)2024
Emodin alleviates intestinal ischemia-reperfusion injury through antioxidant stress, anti-inflammatory responses and anti-apoptosis effects via Akt-mediated HO-1 upregulation.
Article in Journal of inflammation (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Review
- Tranexamic acid inhibits mitochondrial DNA release and reduces inflammatory response in an in vitro model of OGD/R-induced Caco-2 cell injury.BMC pharmacology & toxicology · 2026Article
- Reduced SNHG16 promotes sepsis-induced intestinal injury via the miR-15a-5p/AKT3 axis.BMC gastroenterology · 2026Article
- Article
- Pharmacological strategies for intestinal ischemia-reperfusion injury: mechanisms and therapeutic advances.Frontiers in pharmacology · 2026Review
- Neutrophil extracellular traps drive osteoporosis via NCF2-dependent signaling: integrated transcriptomics with mechanistic validation.Redox report : communications in free radical research · 2025Article
- Mitochondrial function in intestinal ischemia-reperfusion injury: mechanisms and therapeutic perspectives.Molecular biology reports · 2025Review
- Antioxidant and Anti-Inflammatory Activities of Methanol Extract ofInternational journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundIntestinal ischemia-reperfusion (I/R) injury is a severe vascular emergency. Previous research indicated the protective effects of Emodin on I/R injury. Our study aims to explore the effect of Emodin on intestinal I/R (II/R) injury and elucidate the underlying mechanisms.
methodsC57BL/6 mice and Caco-2 cells were used for in vivo and in vitro studies. We established an animal model of II/R injury by temporarily occluding superior mesenteric artery. We constructed an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model using a hypoxia-reoxygenation incubator. Different doses of Emodin were explored to determine the optimal therapeutic dose. Additionally, inhibitors targeting the protein kinase B (Akt) or Heme oxygenase-1 (HO-1) were administered to investigate their potential protective mechanisms.
resultsOur results demonstrated that in animal experiments, Emodin mitigated barrier disruption, minimized inflammation, reduced oxidative stress, and inhibited apoptosis. When Akt or HO-1 was inhibited, the protective effect of Emodin was eliminated. Inhibiting Akt also reduced the level of HO-1. In cell experiments, Emodin reduced inflammation and apoptosis in the OGD/R cell model. Additionally, when Akt or HO-1 was inhibited, the protective effect of Emodin was weakened.
conclusionsOur findings suggest that Emodin may protect the intestine against II/R injury through the Akt/HO-1 signaling pathway.
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