ArticleThe Journal of international medical research2025
Article in The Journal of international medical 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.
- Escin Attenuates Amyloid Beta 1-42-Induced Oxidative Stress, Apoptosis, and Neuroinflammation in Neuron-Like SH-SY5Y Cells.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
ObjectiveThis study aimed to investigate the protective effects of β-escin against neuroinflammatory injury and its influence on the interleukin-6/Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway in a rat model of ischemic stroke.MethodsRats underwent a 2-h middle cerebral artery occlusion and were categorized into sham, middle cerebral artery occlusion, and middle cerebral artery occlusion treated with β-escin (0.45, 0.90, and 1.80 mg/kg) groups. Cerebral damage was assessed using 2,3,5-triphenyltetrazolium chloride and hematoxylin and eosin staining; neuronal apoptosis was evaluated via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay; serum levels of inflammatory cytokines (interleukin-6, tumor necrosis factor-α, and interleukin-1β) were measured using enzyme-linked immunosorbent assay, and protein expression of the interleukin-6/Janus kinase 2/signal transducer and activator of transcription 3 pathway was analyzed using western blot.Resultsβ-escin administration dose-dependently reduced Longa scores, cerebral infarction volume, and pathological damage while also attenuating neuronal apoptosis. It significantly suppressed the release of proinflammatory cytokines and downregulated the expression of interleuin-6 and interleukin-6 receptor as well as the ratios of phosphorylated Janus Kinase 2/Janus Kinase 2 and phosphorylated signal transducer and activator of transcription 3/ signal transducer and activator of transcription 3. These protective effects were positively correlated with the dosage of β-escin.ConclusionThe findings suggested that β-escin exerted neuroprotective effects in ischemic stroke by modulating the interleukin-6/Janus kinase 2/signal transducer and activator of transcription 3 pathway, thereby reducing neuroinflammation and apoptosis.
Indexed as
Identifiers
What 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.