ArticleReproductive sciences (Thousand Oaks, Calif.)2025
The Effect of Ferulic Acid on the Akt-GSK3β Signaling Pathway, Neuroinflammation, Oxidative Stress, and Cortical Damage in the Fetal Brain with Uteroplacental Insufficiency.
Article in Reproductive sciences (Thousand Oaks, Calif.), 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uteroplacental insufficiency (UPI) disrupts fetal brain development and induces oxidative damage. This study evaluates the neuroprotective effects of ferulic acid (FA) on oxidative stress biomarkers, neuroinflammation, the Akt/GSK-3β signaling pathway, and neuronal density in the medial prefrontal cortex (mPFC) following UPI in rats. Twenty pregnant Wistar rats were randomly assigned to four groups: Control, Sham Surgery, UPI + Vehicle (UPI + normal saline), and UPI + FA (UPI + FA at 100 mg/kg). UPI was induced via permanent ligation of the uterine arteries on embryonic day (ED) 18. FA or normal saline was administered orally from ED14 to ED21. On ED21, fetal brain tissue was analyzed for oxidative stress biomarkers (8-hydroxy-2'-deoxyguanosine, protein carbonyl, 4-hydroxy-2-nonenal, and malondialdehyde), inflammatory cytokines (interleukin-6 [IL-6], IL-1β, tumor necrosis factor-alpha [TNF-α], and IL-10), Akt/GSK-3β gene expression, and neuronal density in the mPFC. FA treatment significantly reduced oxidative stress biomarkers and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) while decreasing GSK-3β expression and increasing Akt expression. Additionally, FA enhanced neuronal density in the mPFC and elevated IL-10 levels compared to the UPI + Vehicle group (p < 0.05). Pre-treatment with FA prior to UPI induction mitigated oxidative stress, modulated the Akt/GSK-3β signaling pathway, suppressed neuroinflammation, and preserved cortical integrity in the fetal brain.
Indexed as
Identifiers
41239166What 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.