ArticleDrug design, development and therapy2018
3-
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- Human urinary kallidinogenase or edaravone combined with butylphthalide in the treatment of acute ischemic stroke.Brain and behavior · 2019Trial
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- Sequential release ofMaterials today. Bio · 2026Article
- DL-3-n-Butylphthalide Protects Against PrPCNS neuroscience & therapeutics · 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
- Dl-3-ACS chemical neuroscience · 2025Article
- Spatial metabolic analysis of the regulatory effects of DL-3-n-butylphthalide in a cerebral ischemia-reperfusion mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Wedelolactone Ameliorates Ischemic Stroke by Inhibiting Oxidative Damage and Ferroptosis via HIF-1α/SLC7A11/GPX4 Signaling.Drug design, development and therapy · 2025Article
- Long-Term Benefits of N-Butylphthalide in Preventing Ischemic Stroke Recurrence: A 12-Month Prospective Study.Therapeutics and clinical risk management · 2025Article
- Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Geraniol attenuates oxygen-glucose deprivation/reoxygenation-induced ROS-dependent apoptosis and permeability of human brain microvascular endothelial cells by activating the Nrf-2/HO-1 pathway.Journal of bioenergetics and biomembranes · 2024Article
- Dl-3-n-butylphthalide promotes angiogenesis in ischemic stroke mice through upregulating autocrine and paracrine sonic hedgehog.Acta pharmacologica Sinica · 2023Article
- Dl-3-n-butylphthalide exerts neuroprotective effects by modulating hypoxia-inducible factor 1-alpha ubiquitination to attenuate oxidative stress-induced apoptosis.Neural regeneration research · 2023Article
- Proteomic Analysis of Protective Effects of Dl-3-n-Butylphthalide against mpp + -Induced Toxicity via downregulating P53 pathway in N2A Cells.Proteome science · 2023Article
- Effect of Dl-3-n-butylphthalide on mitochondrial Cox7c in models of cerebral ischemia/reperfusion injury.Frontiers in pharmacology · 2023Article
- The Role of Nrf2 in Relieving Cerebral Ischemia-Reperfusion Injury.Current neuropharmacology · 2023Review
- Article
- Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review).International journal of molecular medicine · 2022Review
- Role of Butylphthalide in Immunity and Inflammation: Butylphthalide May Be a Potential Therapy for Anti-Inflammation and Immunoregulation.Oxidative medicine and cellular longevity · 2022Review
- Knockdown of ILK Alleviates High Glucose-Induced Damage of H9C2 Cells through TLR4/MyD88/NF-Disease markers · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study examined whether the neuroprotective drug, 3- MATERIALS AND
methodsPC12 neuronal cells were pretreated for 24 hours with NBP (10 μmol/L), then exposed to oxygen and glucose deprivation (OGD) for 8 hours as an in vitro model of ischemic stroke. Indices of anti-oxidative response, mitochondrial function and mitochondrial dynamics were evaluated.
resultsOGD suppressed cell viability, induced apoptosis and increased caspase-3 activity. NBP significantly reversed these effects. NBP prevented oxidative damage by increasing the activity of superoxide dismutase and lowering levels of malondialdehyde (MDA) and reactive oxygen species (ROS). At the same time, it increased expression of Nrf2, HO-1 and AMPK. NBP attenuated mitochondrial dysfunction by enhancing mitochondrial membrane potential and increasing the activity of mitochondrial respiratory chain complexes I-IV and ATPase. NBP altered the balance of proteins regulating mitochondrial fusion and division.
conclusionNBP exerts neuroprotective actions by enhancing anti-oxidation and attenuating mitochondrial dysfunction. Our findings provide insight into how NBP may exert neuroprotective effects in ischemic stroke and raise the possibility that it may function similarly against other neurodegenerative diseases involving mitochondrial dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.