ArticleToxicology research2024
Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury by regulating miR-4454.
Article in Toxicology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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Who cites it
1 citing paper in PubMed.
- Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via the LncRNA FAM201A/miR-488-3p/PTEN axis.BMC anesthesiology · 2025Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSevoflurane (Sevo) prevents hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. The expression of miR-4,454 was increased in individuals experiencing an acute myocardial infarction.
objectiveThe purpose of current investigation was to delved into whether the effects of Sevo on cardiomyocytes are mediated through regulation of miR-4,454 expression.
methodIn this study, the expression levels of miR-4,454 and BAG5 were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability was detected by cell counting kit-8 (CCK-8). The levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) were detected by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were detected using various commercially available kits to assess the level of oxidative stress in the cells. The luciferase reporter gene assay was used to verify the interaction of miR-4,454 with downstream target genes.
resultsThere was a notable upregulation of miR-4,454 expression in H/R-induced cardiomyocyte models. This was accompanied by a decrease in the viability of myocardial cells induced by H/R and an intensification of the extent of myocardial injury and oxidative stress. However, the detrimental effects were mitigated by the administration of Sevo. miR-4,454 had a target site for binding to BAG5, and its expression was negatively modulated by miR-4,454. An increase in the expression of BAG5 was shown to directly offset the exacerbation of cardiomyocyte damage induced by the overexpression of miR-4,454.
conclusionSevo may attenuate H/R-induced cardiomyocyte injury by regulating miR-4454.
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