ArticleFrontiers in pharmacology2025
The SAP130/Mincle axis was involved in sevoflurane-induced neuronal death and microglial activation in juvenile mice.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Sevoflurane is widely used in pediatric anesthesia and has raised concerns for years regarding its neurotoxic effects on the developing brain. Studies have shown that sevoflurane can lead to neuronal cell death and neuroinflammation, which further contribute to sevoflurane-induced neurotoxicity manifested as delirium or cognitive deficits. However, the molecular mechanism remains poorly understood. A factor of interest is Sin3A-associated protein 130 (SAP130), which can be released by dead or damaged cells and trigger sterile inflammation, exacerbating tissue damage by activating the macrophage-inducible C-type lectin (Mincle) receptor. However, whether the SAP130/Mincle axis is involved in sevoflurane-induced neurotoxicity remains unknown. Methods: Using a young murine sevoflurane exposure model and a primary neuron-microglia co-culture system, we examined changes in neuronal cell death, microglial activation, cytokine production, and the expression levels of SAP130- and Mincle-signaling-associated proteins after sevoflurane exposure. We then applied SAP130-neutralizing antibody and the Syk inhibitor piceatannol to assess the impact of inhibiting the Mincle pathway on microglial activation and sevoflurane-induced neurotoxicity. Results: The results demonstrated that sevoflurane exposure increased the number of dead neurons with SAP130 upregulation and induced microglial activation with cytokine production in the hippocampus. These changes occurred only in the neuron-microglia co-culture system but not in neuron or microglia monoculture. Neutralizing SAP130 or pharmacologically inhibiting syk diminished microglial activation and neuronal cell death by suppressing the SAP130/Mincle signaling pathway. Discussion: These findings suggest that the SAP130/Mincle axis plays a crucial role in neuronal death and microglial activation in sevoflurane-induced neurotoxicity. Targeting this axis emerges as a potential therapeutic strategy to mitigate the neurotoxic effects of sevoflurane.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.