ArticleScientific reports2025
In vivo and in vitro investigations of schisandrin B against angiotensin II induced ferroptosis and atrial fibrosis by regulation of the SIRT1 pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Schisandrin B targets CD44 to inhibit glioblastoma multiforme.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Article
- SLC7A11 in Fibrosis: Molecular Mechanisms and Future Prospects.Aging and disease · 2025Review
- Integrative UHPLC-HRMS and computational biology reveal ferroptosis and anoikis targeting by Wenpitongluo decoction in cardiorenal syndrome.Frontiers in chemistry · 2025Article
- Traditional Chinese medicine and plant-derived bioactive compounds as sustainable alternatives to antibiotics in bovine mastitis: a review.Frontiers in veterinary science · 2025Review
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Authors and funding
2 authors.
Funding
Abstract
Schisandrin B (Sch B) derived from Schisandra chinensis, is known for its anti-inflammatory and anti-microbial properties. The study aimed to explore Sch B's protective roles and underlying mechanisms in angiotensin II (Ang II) - induced ferroptosis, atrial fibrosis, and AF using both in vivo and in vitro models. AF mice model generated induced by Ang II and established an in vitro model using the HL-1 cell line induced by Ang II. We assessed atrial fibrosis through histological analysis and oxidative stress analysis. We employed RT-qPCR and Western blot techniques to evaluate mRNA and protein expression. Sch B significantly attenuated Ang II-induced AF development, atrial apoptosis, and myocardial injury-related molecules, including CK-MB and LDH. Relative DHE intensity, MDA, NOX2, and NOX4 increased significantly, and SOD and CAT levels decreased markedly in Ang II-induced mice. Sch B treatment could inhibit atrial ROS production and oxidative stress in Ang II-infused mice. In addition, Sch B showed cardioprotective effects in Ang II-infused HL-1 cells. Sch B significantly reduced pro-inflammatory cytokines, including IL-1β, TNF-α, and IL-6, restored by EX527 (SIRT1 inhibitor). Sch B inhibited intracellular ROS generation and oxidative stress in HL-1 cells, which were restored by Ex-527. Furthermore, Sch B decreased the increase in Fe2 + concentration caused by Ang II infusion, which was recovered by Ex-527. Sch B markedly increased the expression of SIRT1, SLC7A11, GPX4 and FTH1 while reducing the expression patterns by Ex-527 treatment. Our experimental data suggest that Sch B protects against Ang II-induced ferroptosis, atrial fibrosis, and AF by activating SIRT1 in vivo and in vitro.
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