ArticleNeural regeneration research2023
Withaferin A inhibits ferroptosis and protects against intracerebral hemorrhage.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Network pharmacology, molecular docking, and experimental validation of the mechanisms of Withaferin a in treating periodontitis.Clinical oral investigations · 2026Article
- Plant-Derived Natural Compounds and Nrf2-Centered Redox Signaling in Intracerebral Hemorrhage: Evidence Grading, Mechanistic Boundaries, and Translational Challenges.Antioxidants (Basel, Switzerland) · 2026Review
- Matrine Attenuates Neurological Deficits and Neuroinflammation by Inhibiting the HMGB1/RAGE Axis and Ferroptosis in Intracerebral Hemorrhage Mice.The Kaohsiung journal of medical sciences · 2026Article
- Microglial Membranes Wrapped Ultrasmall Medium-Entropy Ru Single-Atom Nanozyme: Enhanced Catalysis for Accelerating Inflammation/Redox Microenvironment Regulation in Intracerebral Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Betaine Inhibits Ferroptosis After Intracerebral Hemorrhage by Activating the Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Methotrexate-triggered ferroptosis suppresses oral cancer progression by phosphorylated KEAP1-mediated NRF2 degradation to inhibit SLC7A11/GPX4 signaling pathway.Cancer cell international · 2026Article
- A Self-Assembling Nanomodulator for Synergistic Therapy of Intracerebral Hemorrhage.International journal of nanomedicine · 2026Article
- Ferroptosis inhibitors: mechanisms of action and therapeutic potential.Cellular and molecular life sciences : CMLS · 2025Review
- Esculetin inhibits ferroptosis after ICH by promoting NUDT1-mediated m7G methylation modification of GPX4.Scientific reports · 2025Article
- Eupatilin mitigates ICH-induced brain injury via SOX2/SLC7A11 regulation of ferroptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- BRD4 silencing attenuates hemin-induced neuronal ferroptosis and inflammation via the H3K27ac-ATF3 axis in an in vitro model of cerebral hemorrhage.European journal of medical research · 2025Article
- Baicalin plays a protective role by regulating ferroptosis in multiple diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- PF4 regulates neuronal ferroptosis in cerebral hemorrhage through CXCR3/PI3K/AKT/Nrf2 pathway.Biomolecules & biomedicine · 2025Article
- Analysis of ferroptosis-related genes in cerebral ischemic stroke via immune infiltration and single-cell RNA-sequencing.BMC medical genomics · 2025Article
- New targets in spontaneous intracerebral hemorrhage.Current opinion in neurology · 2025Review
- Ferroptosis-associated pathological injury mechanisms and therapeutic strategies after intracerebral hemorrhage.Frontiers in neurology · 2025Review
- Beyond oxidative stress: Ferroptosis as a novel orchestrator in neurodegenerative disorders.Frontiers in immunology · 2025Review
- Targeting ferroptosis with natural products in stroke: therapeutic mechanisms and translational opportunities.Frontiers in pharmacology · 2025Review
- Traditional Chinese Medicine and Ferroptosis in Intracerebral Hemorrhage: A Potential Therapeutic Approach.Drug design, development and therapy · 2025Review
- EGCG activates Keap1/P62/Nrf2 pathway, inhibits iron deposition and apoptosis in rats with cerebral hemorrhage.Scientific reports · 2024Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have indicated that suppressing oxidative stress and ferroptosis can considerably improve the prognosis of intracerebral hemorrhage (ICH). Withaferin A (WFA), a natural compound, exhibits a positive effect on a number of neurological diseases. However, the effects of WFA on oxidative stress and ferroptosis-mediated signaling pathways to ICH remain unknown. In this study, we investigated the neuroprotective effects and underlying mechanism for WFA in the regulation of ICH-induced oxidative stress and ferroptosis. We established a mouse model of ICH by injection of autologous tail artery blood into the caudate nucleus and an in vitro cell model of hemin-induced ICH. WFA was injected intracerebroventricularly at 0.1, 1 or 5 µg/kg once daily for 7 days, starting immediately after ICH operation. WFA markedly reduced brain tissue injury and iron deposition and improved neurological function in a dose-dependent manner 7 days after cerebral hemorrhage. Through in vitro experiments, cell viability test showed that WFA protected SH-SY5Y neuronal cells against hemin-induced cell injury. Enzyme-linked immunosorbent assays in vitro and in vivo showed that WFA markedly decreased the level of malondialdehyde, an oxidative stress marker, and increased the activities of anti-oxidative stress markers superoxide dismutase and glutathione peroxidase after ICH. Western blot assay, quantitative polymerase chain reaction and immunofluorescence results demonstrated that WFA activated the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling axis, promoted translocation of Nrf2 from the cytoplasm to nucleus, and increased HO-1 expression. Silencing Nrf2 with siRNA completely reversed HO-1 expression, oxidative stress and protective effects of WFA. Furthermore, WFA reduced hemin-induced ferroptosis. However, after treatment with an HO-1 inhibitor, the neuroprotective effects of WFA against hemin-induced ferroptosis were weakened. MTT test results showed that WFA combined with ferrostatin-1 reduced hemin-induced SH-SY5Y neuronal cell injury. Our findings reveal that WFA treatment alleviated ICH injury-induced ferroptosis and oxidative stress through activating the Nrf2/HO-1 pathway, which may highlight a potential role of WFA for the treatment of ICH.
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