ArticleExperimental brain research2025
Dexmedetomidine alleviates sevoflurane-induced neurotoxicity during late pregnancy by modulating apoptotic pathways and BDNF receptor expression.
Article in Experimental brain research, 2025. 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
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
1 citing paper in PubMed.
- Bioengineered human brain organoids and organ-on-chip platforms for exposure-aware assessment of developmental neurotoxicity induced by general anesthetics and sedatives.Frontiers in bioengineering and biotechnology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
To investigate the associations between the neurotoxicity of sevoflurane and the neuroprotection provided by dexmedetomidine, we measured apoptotic gene and protein expression, brain-derived neurotrophic factor (BDNF) levels, and receptor expression, and neuronal apoptosis. Pregnant rats were treated with dexmedetomidine, 2.5% sevoflurane for 6 h, or a combination of 2.5% sevoflurane for 6 h with dexmedetomidine on gestational day 18 (G18). The apoptotic genes and proteins expression, BDNF and receptor expression, and neuronal apoptosis were assessed in offspring hippocampi on postnatal day 1 (P1) and P41. Dendritic spine density, synaptophysin protein fluorescence staining, and cognitive function were evaluated on P41. Maternal sevoflurane exposure increased Bax mRNA and protein expression, decreased Bcl-2 mRNA and protein expression, enhanced neuronal apoptosis, decreased the ratio of mature BDNF (mBDNF) to proBDNF, reduced mBDNF and tropomyosin receptor kinase B (TrkB) protein expression, and increased p75 neurotrophin receptor (p75NTR) protein expression in the hippocampi of neonatal rats. In juvenile rats, maternal sevoflurane exposure reduced mBDNF and TrkB protein expression, dendritic spine density, the proportion of time spent in the target quadrant, and the number of crossings over the platform while increasing escape latency in the Morris water maze. All abnormalities induced by maternal sevoflurane exposure, except for mBDNF levels on P41, were alleviated by dexmedetomidine. Dexmedetomidine mitigates sevoflurane-induced neuronal development abnormalities and cognitive impairments during late pregnancy by improving hippocampal Bcl-2 and Bax mRNA and protein expression, as well as proBDNF-p75NTR and mBDNF-TrkB protein expression in offspring.
Indexed as
Identifiers
40116959What Socratic 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 Socratic graph.