ArticleNeural regeneration research2023
Dl-3-n-butylphthalide exerts neuroprotective effects by modulating hypoxia-inducible factor 1-alpha ubiquitination to attenuate oxidative stress-induced apoptosis.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Butylphthalide enhances neurorestoration following ischemic stroke by restructuring microvasculature through vimentin modulation.Journal of advanced research · 2026Article
- Sequential release ofMaterials today. Bio · 2026Article
- Layered Double Hydroxide-Loaded Dl-3-n-Butylphthalide Alleviates Renal Ischemia-Reperfusion Injury by Regulating the PI3K-AKT-Nrf2 Signaling Pathway.International journal of nanomedicine · 2026Article
- DL-3-n-Butylphthalide Protects Mitochondria Against Ischemia/Hypoxia Damage via Suppressing GCN5L1-Mediated Drp1 Acetylation in Neurons and Mouse Brains.CNS neuroscience & therapeutics · 2025Article
- Contribution and Regulation of HIF-1α in Testicular Injury Induced by Diabetes Mellitus.Biomolecules · 2025Review
- Neuronal regulated cell death in aging-related neurodegenerative diseases: key pathways and therapeutic potentials.Neural regeneration research · 2025Article
- Investigation of the Impact Factors and Efficacy of N-Butylphthalide (NBP) on Functional Outcomes Following Mechanical Thrombectomy in Stroke Patients.International journal of general medicine · 2025Article
- Long-Term Benefits of N-Butylphthalide in Preventing Ischemic Stroke Recurrence: A 12-Month Prospective Study.Therapeutics and clinical risk management · 2025Article
- Long-term exposure to PMScientific reports · 2024Article
- [Expression and significance of hypoxia-inducible factor 1α and Bcl-2/adenovirus E1B19kDa-interacting protein 3 in children with traumatic brain injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Review
- Unveiling the potential of Butylphthalide: inhibiting osteoclastogenesis and preventing bone loss.Frontiers in pharmacology · 2024Article
- The mitochondria as a potential therapeutic target in cerebral I/R injury.Frontiers in neuroscience · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dl-3-n-butylphthalide is used to treat mild and moderate acute ischemic stroke. However, the precise underlying mechanism requires further investigation. In this study, we investigated the molecular mechanism of Dl-3-n-butylphthalide action by various means. We used hydrogen peroxide to induce injury to PC12 cells and RAW264.7 cells to mimic neuronal oxidative stress injury in stroke in vitro and examined the effects of Dl-3-n-butylphthalide. We found that Dl-3-n-butylphthalide pretreatment markedly inhibited the reduction in viability and reactive oxygen species production in PC12 cells caused by hydrogen peroxide and inhibited cell apoptosis. Furthermore, Dl-3-n-butylphthalide pretreatment inhibited the expression of the pro-apoptotic genes Bax and Bnip3. Dl-3-n-butylphthalide also promoted ubiquitination and degradation of hypoxia inducible factor 1α, the key transcription factor that regulates Bax and Bnip3 genes. These findings suggest that Dl-3-n-butylphthalide exhibits a neuroprotective effect on stroke by promoting hypoxia inducible factor-1α ubiquitination and degradation and inhibiting cell apoptosis.
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Registered trials
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