ArticleMolecular medicine reports2016
Intestinal ischemic preconditioning reduces liver ischemia reperfusion injury in rats.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Disrupting cell death: ferroptosis and pyroptosis inhibition in hepatic ischemia-reperfusion injury via modulation of GPX4 and cGAS pathways by deferoxamine and octreotide.Frontiers in pharmacology · 2025Article
- Mitochondrial Dysfunction and Oxidative Stress in Liver Transplantation and Underlying Diseases: New Insights and Therapeutics.Transplantation · 2021Review
- A Dual Protective Effect of Intestinal Remote Ischemic Conditioning in a Rat Model of Total Hepatic Ischemia.Journal of clinical medicine · 2019Article
- Pre-conditions for eliminating mitochondrial dysfunction and maintaining liver function after hepatic ischaemia reperfusion.Journal of cellular and molecular medicine · 2017Review
- Current Antioxidant Treatments in Organ Transplantation.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the current study was to investigate whether intestinal ischemic preconditioning (IP) reduces damage to the liver during hepatic ischemia reperfusion (IR). Sprague Dawley rats were used to model liver IR injury, and were divided into the sham operation group (SO), IR group and IP group. The results indicated that IR significantly increased Bax, caspase 3 and NF‑κBp65 expression levels, with reduced expression of Bcl‑2 compared with the IP group. Compared with the IR group, the levels of AST, ALT, MPO, MDA, TNF‑α and IL‑1 were significantly reduced in the IP group. Immunohistochemistry for Bcl‑2 and Bax indicated that Bcl‑2 expression in the IP group was significantly increased compared with the IR group. In addition, IP reduced Bax expression compared with the IR group. The average liver injury was worsened in the IR group and improved in the IP group, as indicated by the morphological evaluation of liver tissues. The present study suggested that IP may alleviates apoptosis, reduce the release of pro‑inflammatory cytokines, ameloriate reductions in liver function and reduce liver tissue injury. To conclude, IP provided protection against hepatic IR injury.
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Registered trials
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