ArticleToxicology reports2025
Phenolic-rich fraction of
Article in Toxicology reports, 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
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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
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.
- Protective Effects of Policosanol and Atorvastatin Co-Supplementation Against High-Cholesterol and High-Galactose Diet-Induced Metabolic and Organ Dysfunction in Zebrafish.International journal of molecular sciences · 2026Article
- Combination of Policosanol (RaydelPharmaceuticals (Basel, Switzerland) · 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
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atorvastatin, a widely prescribed cholesterol-lowering medication, has been linked to statin-induced myotoxicity, a condition marked by elevated muscle enzymes and oxidative stress. While statins are essential for managing hypercholesterolemia and preventing cardiovascular diseases, their myotoxic side effects limit broader clinical use. This study investigated the myo-protective effects of the phenolic-rich fraction of Methods: Thirty female Wistar rats were divided into five groups: (1) a true control group receiving distilled water, (2) an atorvastatin-only group, and three treatment groups receiving PRFSB at varying doses (100, 200, and 400 mg/kg) alongside atorvastatin. Muscle enzymes (creatine kinase and lactate dehydrogenase), oxidative stress markers (catalase, superoxide dismutase, and malondialdehyde), and histopathological changes were assessed. Results: Atorvastatin significantly elevated serum CK, LDH and oxidative stress markers, while PRFSB administration, particularly at 400 mg/kg, significantly reduced these elevations (p < 0.05). PRFSB restored muscle enzyme levels, normalized antioxidant defenses and reduced lipid peroxidation. Histological analysis revealed that PRFSB-treated groups exhibited preserved muscle architecture with minimal inflammation. Conclusion: PRFSB effectively alleviated atorvastatin-induced myotoxicity by reducing oxidative stress, restoring muscle biomarkers and protecting tissue integrity. These findings suggest that PRFSB holds promise as an adjunct therapy to mitigate statin-induced muscle toxicity, warranting further exploration in clinical settings.
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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.