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- Title
Emodin alleviates intestinal ischemia–reperfusion injury through antioxidant stress, anti-inflammatory responses and anti-apoptosis effects via Akt-mediated HO-1 upregulation.
- Authors
Liu, Yinyin; Ji, Tuo; Jiang, Haixing; Chen, Meng; Liu, Wanli; Zhang, Zongze; He, Xianghu
- Abstract
Background: Intestinal 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. Methods: C57BL/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. Results: Our 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. Conclusions: Our findings suggest that Emodin may protect the intestine against II/R injury through the Akt/HO-1 signaling pathway.
- Subjects
EMODIN; INTESTINAL injuries; REPERFUSION injury; PROTEIN kinase B; PROTEIN kinase inhibitors; MESENTERIC artery
- Publication
Journal of Inflammation, 2024, Vol 21, Issue 1, p1
- ISSN
1476-9255
- Publication type
Article
- DOI
10.1186/s12950-024-00392-z