ArticleJournal of thoracic disease2017
Protective effect of propofol preconditioning on ischemia-reperfusion injury in human hepatocyte.
Article in Journal of thoracic disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Effect of different anaesthetic techniques on gene expression profiles in patients who underwent hip arthroplasty.PloS one · 2019Trial
- Sevoflurane exerts improved protective effects than propofol on hypoxia-reoxygenation injury by regulating the microRNA-221-5p/ADAM8 axis in cardiomyocytes.Experimental and therapeutic medicine · 2021Article
- Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury.The Journal of international medical research · 2021Article
- Effects of remifentanil and propofol on distant organ lung injury in an ischemia-reperfusion model.Open medicine (Warsaw, Poland) · 2021Article
- Propofol-induced MiR-20b expression initiates endogenous cellular signal changes mitigating hypoxia/re-oxygenation-induced endothelial autophagy in vitro.Cell death & disease · 2020Article
- Inhaled Argon Impedes Hepatic Regeneration after Ischemia/Reperfusion Injury in Rats.International journal of molecular sciences · 2020Article
- Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways.Experimental and therapeutic medicine · 2020Article
- Effects of propofol combined with remifentanil anesthesia on the NO, endothelin and inflammatory cytokines in the plasma of patients with liver cirrhosis during the perioperative period.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBlood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism.
methodsWistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 µmol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis.
resultsALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning.
conclusionsOur findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/R injury, which might provide a scientific basis for clinical application.
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