ArticleBMC pharmacology & toxicology2025
Obeticholic acid prevents cyclophosphamide-induced placental injury via SIRT1 and TLR4/NF-κB pathways.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Obeticholic acid attenuates complete freund's adjuvant-induced arthritis in rats through FXR-mediated modulation of TGF-β/TAK1/MKK3/p38 MAPK signaling, inflammation, and oxidative stress.Inflammopharmacology · 2026Article
- Obeticholic Acid and Edaravone Protect Against Cisplatin-Induced Hepatotoxicity Through Modulation of Keap1/Nrf2/ARE, TNF-α/NF-κB, and AKT/GSK-3β Pathways.Journal of biochemical and molecular toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of the current study is to identify the possible protective effect of obeticholic acid (OCA) on placental injury caused by cyclophosphamide (CP). OCA was administered in the presence and absence of CP.
methodsThirty-two pregnant female rats were randomly assigned to four groups: control group, OCA group: received OCA (10 mg/kg /day, orally), CP group: received CP 20 mg/kg intraperitoneally at 12th day, OCA + CP group. Placental weight and placental growth factor (PlGF) were measured. Placental oxidative stress parameters (malondialdahide (MDA) and total antioxidant capacity (TAC)), besides Sirtuin type 1 (SIRT1), nuclear factor erythroid 2-related factor 2 (Nrf2), myeloid differentiation factor 88 (Myd88) and caspase-3 biomarkers, were evaluated. Nuclear factor-kappa B (NF-κB) and tumor necrosis factor-alpha (TNF-α) gene expression were also measured. Placental histopathological examination, toll- like receptor4 (TLR4) and forkhead-box transcription factor1 (FOXO1) immunohistochemical study were performed.
resultsCP significantly decreased PlGF, placental weight, TAC, SIRT1 and Nrf2 with increased placental MDA, Myd88, caspase-3, NF-κB and TNF-α. Histopathological findings of placental damage and high TLR4, FOXO1 immunoexpressions were detected. OCA significantly increased PlGF level, placental weight and normalized the distributed oxidative stress, inflammatory, and apoptotic biomarkers with a prompt improvement in the histopathological picture and decrease TLR4 and FOXO1 immunoexpressions.
conclusionAccordingly, these findings suggest that OCA protects CP-induced placental injury by modulating TLR4/Myd88/NF-κB; SIRT1-dependant signaling pathways.
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.