ArticleMolecular biology reports2026
Rutin attenuates acrylamide-induced oxidative liver injury.
Article in Molecular biology reports, 2026. 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
backgroundAcrylamide (ACR) is an important chemical raw material, and its toxic effects have been confirmed in vitro and in vivo. However, only a few studies have investigated ACR-induced liver injury. As a naturally occurring flavonoid widely distributed across the plant kingdom, rutin (Rut) possesses notable pharmacological properties. This study aimed to demonstrate its therapeutic potential in mitigating ACR-induced hepatic injury in rats. Accordingly, an intervention model was established to explore the mechanistic basis of the protective effects of Rut against ACR-induced liver injury.
methodsThe experimental design comprised five cohorts (n = 10), consisting of 50 male Sprague-Dawley rats randomly assigned to each group: (1) Control (0.5% CMC-Na + ddH
resultsCompared with the Control group, ACR exposure attenuated the rate of body weight accrual (P < 0.05) and the liver-to-body weight ratio (P < 0.05), elevated serum ALT (↑34.8%, P < 0.05) and AST (↑47.7%, P < 0.05), decreased hepatic SOD (↓48.9%, P < 0.05) and GSH (↓17.7%, P < 0.05), and increased MDA (↑38.8%, P < 0.05). High-dose Rut reversed these effects by increasing body weight gain (P < 0.01), liver coefficient (↑29.4%, P < 0.05), SOD (↑32.1%, P < 0.05), and GSH (↑12.1%, P < 0.05), while reducing ALT (↓22.9%, P < 0.01), AST (↓16.8%, P < 0.01), and MDA (↓9.0%, P < 0.05) levels. Histopathological analysis demonstrated reduced hepatocyte necrosis and collagen deposition in the Rut-treated group. Immunohistochemistry revealed that ACR increased TNF-α (↑121.4%, P < 0.001) and cleaved caspase-3 (↑97.8%, P < 0.001) expression, which was suppressed by Rut (TNF-α: ↓48.2%, P < 0.01; cleaved caspase-3: ↓39.5%, P < 0.01). The effect sizes (Cohen's d) ranged from 1.2 to 3.6, indicating robust effects.
conclusionRut exhibits a marked protective effect against ACR-induced hepatic injury. Therefore, Rut may be considered a potential agent for preventing ACR-induced liver injury in rats.
Indexed as
Identifiers
42525287What 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.