ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Alpha-pinene protects rat liver against acetaminophen-induced oxidative stress and apoptosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Scoparone protects against acetaminophen-induced acute liver injury: Insights from In vivo experiments and RNA sequencing.Biochemistry and biophysics reports · 2026Article
- Chemical Characterization and Rumen-Modulating Effects ofMolecules (Basel, Switzerland) · 2026Article
- Protective Effects ofFood science & nutrition · 2026Article
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Authors and funding
5 authors.
Funding
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Abstract
Acetaminophen (APA) is a commonly used antipyretic and analgesic medication worldwide. The current study aims to investigate the relationship between alpha-pinene, oxidative stress factors, genes involved in the apoptotic pathway, and liver damage caused by PAR. Thirty Wistar rats were divided into five groups: a control group and four treatment groups receiving APA (0.640 g/kg/day), APA+alpha-pinene (75 mg/kg), APA+alpha-pinene (125 mg/kg), and APA+ silymarin (50 mg/kg). The treatment groups were injected with APA for 2 weeks, while the control group received distilled water. The study assessed liver enzymes, oxidative stress factors, and apoptotic gene expression. We found that alpha-pinene decreased the ALT, AST, and ALP levels in the liver of PAR-treated rats. Alpha-pinene restored GSH, MDA, SOD, and CAT activities in the liver of PAR-treated rats. Real-time PCR analysis showed that alpha-pinene inhibited apoptosis by suppressing Bax and caspase-3 and upregulating Bcl-2 in the liver of APA-treated rats. Moreover, alpha-pinene downregulates PPARγ in the liver of APA-treated rats. Alpha-pinene has been discovered to have protective properties against liver damage caused by the use of APA. This protection is achieved by reducing oxidative stress and apoptosis. Alpha-pinene increases the expression of Bcl-2, which has an anti-apoptotic effect and reduces the levels of Bax and caspase-3.
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Registered trials
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