ArticleBMC anesthesiology2024
Remimazolam protects the liver from ischemia-reperfusion injury by inhibiting the MAPK/ERK pathway.
Article in BMC anesthesiology, 2024. 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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Who cites it
5 citing papers in PubMed.
- Discontinuation of the development of remimazolam for ICU sedation in Japan: background and rationale.Journal of intensive care · 2026Review
- Remimazolam in anesthesia and sedation: A narrative review.Journal of anesthesia and translational medicine · 2025Review
- Siglec6 CAR T cells suppressed progression of AML via inhibiting Siglec6 and SHP2 induced Src and ERK signaling activation.Scientific reports · 2025Article
- Remimazolam alleviates hepatic ischemia-reperfusion injury by activating FOXO1/3 signaling : Remimazolam alleviates hepatic ischemia reperfusion injury.BMC gastroenterology · 2025Article
- Remimazolam attenuated lipopolysaccharide-induced behavioral deficits and neuronal injury via activation of the Nrf2 pathway.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundIschemia-reperfusion (I/R) injury is a major factor in liver damage following hepatic resection and liver transplantation, with anesthetics demonstrating the ability to shield organs from this type of injury.
methodsHypoxia-reoxygenation (H/R) was used to create in vitro I/R hepatocyte cell injury models. The CCK-8 assay, flow cytometer, LDH assay, and ELSIA were utilized to assess hepatocyte injury. The in vivo I/R injury rat model was then built. HE and TUNEL staining were used to assess liver tissue damage. Western-blot was applied to assess the activation of the MAPK/ERK pathway.
resultsRemimazolam (RMZL) remarkably improved cell viability and decreased apoptosis in H/R-induced hepatocyte injury. RMZL reduced the release of H/R-induced inflammatory mediators (TNF-α and IL-6) as well as LDH levels. We also discovered that RMZL inhibited p38 and ERK1/2 phosphorylation in vivo and in vitro. The stimulation of MAPK/ERK, on the other hand, abolished RMZL's anti-inflammation effects in H/R-induced hepatocyte injury. Furthermore, RMZL reduced liver tissue injury in I/R rats.
conclusionRMZL prevented hepatic I/R damage by inhibiting MAPK/ERK signaling.
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