ArticleInternational journal of molecular sciences2020
Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Efficacy and Mechanism of Silymarin Extract for Deep Second-Degree Burns in Rats.Chinese journal of integrative medicine · 2026Article
- Flavonoids in natural products for the therapy of liver diseases: progress and future opportunities.Frontiers in pharmacology · 2024Review
- Azadirachtin Attenuates Carcinogen Benzo(a) Pyrene-Induced DNA Damage, Cell Cycle Arrest, Apoptosis, Inflammatory, Metabolic, and Oxidative Stress in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Curcumin Suppresses the Lipid Accumulation and Oxidative Stress Induced by Benzo[a]pyrene Toxicity in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Quercetin and Isorhamnetin Attenuate Benzo[a]pyrene-Induced Toxicity by Modulating Detoxification Enzymes through the AhR and NRF2 Signaling Pathways.Antioxidants (Basel, Switzerland) · 2021Article
- A Review of the Role of Flavonoids in Peptic Ulcer (2010-2020).Molecules (Basel, Switzerland) · 2020Review
- Oxidative Stress and DNA Damage in Chronic Disease and Environmental Studies.International journal of molecular sciences · 2020Article
- Protective Effects of Myricetin on Benzo[a]pyrene-Induced 8-Hydroxy-2'-Deoxyguanosine and BPDE-DNA Adduct.Antioxidants (Basel, Switzerland) · 2020Article
- Aortic Injury Induced by Benzo(a)pyrene and Atherogenic Diet Increased Hepatic FGF21 Expression in C57BL/6J Mice.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, is a group 1 carcinogen that introduces mutagenic DNA adducts into the genome. In this study, we investigated the molecular mechanisms underlying the involvement of silymarin in the reduction of DNA adduct formation by B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE), induced by B[a]P. B[a]P exhibited toxicity in HepG2 cells, whereas co-treatment of the cells with B[a]P and silymarin reduced the formation of BPDE-DNA adducts, thereby increasing cell viability. Determination of the level of major B[a]P metabolites in the treated cells showed that BPDE levels were reduced by silymarin. Nuclear factor erythroid 2-related factor 2 (Nrf2) and pregnane X receptor (PXR) were found to be involved in the activation of detoxifying genes against B[a]P-mediated toxicity. Silymarin did not increase the expression of these major transcription factors, but greatly facilitated their nuclear translocation. In this manner, treatment of HepG2 cells with silymarin modulated detoxification enzymes through NRF2 and PXR to eliminate B[a]P metabolites. Knockdown of Nrf2 abolished the preventive effect of silymarin on BPDE-DNA adduct formation, indicating that activation of the Nrf2 pathway plays a key role in preventing B[a]P-induced genotoxicity. Our results suggest that silymarin has anti-genotoxic effects, as it prevents BPDE-DNA adduct formation by modulating the Nrf2 and PXR signaling pathways.
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Registered trials
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