ArticleJournal of biochemical and molecular toxicology2025
The Protective Effects of Chrysin on Acrylamide-Induced Hepatotoxicity: Insights Into Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histological Evaluation in Rats.
Article in Journal of biochemical and molecular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
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Who cites it
3 citing papers in PubMed.
- Betaine Alleviates Favipiravir-induced Ovarian and Uterine Toxicity by Regulating Oxidative, Inflammatory, Cellular Death, Steroidogenic, Hormonal, and Histopathological Changes.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Rutin attenuates acrylamide-induced oxidative liver injury.Molecular biology reports · 2026Article
- Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study.Journal of molecular neuroscience : MN · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Acrylamide (ACR) is a toxic chemical with a high carcinogenic risk that is released as a result of heating or processing foods at high temperatures. Chrysin (CHR) is a flavonoid that is naturally found in foods such as honey and passionflower and stands out with its antioxidant, anticancer, and anti-inflammatory properties. This study aims to determine the protective effects of CHR in ACR-induced hepatotoxicity. ACR was administered orally at a dose of 38.27 mg/kg; CHR (25 or 50 mg/kg) was administered orally for ten days. Biochemical and molecular methods were used to investigate oxidative stress, inflammation, and apoptotic markers in liver tissue. Additionally, histological methods were used to determine the liver tissue's structural and functional characteristics and autophagy. CHR treatment alleviated ACR-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased oxidant MDA. CHR reduced inflammatory activity by inactivating NF-κB and pro-inflammatory cytokines. ACR-induced increases in apoptotic Casp-3, Casp-6, Casp-9, and Bax were reduced by CHR, while the decreased level of antiapoptotic Bcl-2 was increased. It was also determined immunohistochemically that CHR inhibited autophagic Beclin-1 activity. CHR was effective in reducing ACR-induced hepatotoxicity damage and may be an effective treatment option.
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Registered trials
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