ArticleJournal of biomedical science2017
Dl-3-n-butylphthalide protects the heart against ischemic injury and H9c2 cardiomyoblasts against oxidative stress: involvement of mitochondrial function and biogenesis.
Article in Journal of biomedical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Anti-fibrosis effect of astragaloside IV in animal models of cardiovascular diseases and its mechanisms: a systematic review.Pharmaceutical biology · 2025Pooled it
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Pleiotropic role of GAS6 in cardioprotection against ischemia-reperfusion injury.Journal of advanced research · 2025Article
- Identification of key genes associated with oxidative stress in ischemic stroke via bioinformatics integrated analysis.BMC neuroscience · 2025Article
- The potential mechanism of mitochondrial homeostasis in postoperative neurocognitive disorders: an in-depth review.Annals of medicine · 2024Review
- 3-N-Butylphthalide Confers Antiarrhythmic Features in Ischemia/Reperfusion Injury of Diabetic Heart by Targeting Mitochondria-Endoplasmic Reticulum Network and Inhibiting Oxidative Stress and Inflammation.Physiological research · 2024Article
- Engineered Mitochondrial Transplantation as An Anti-Aging Therapy.Aging and disease · 2024Review
- DL-3-Heliyon · 2024Article
- Taurine promotes axonal sprouting via Shh-mediated mitochondrial improvement in stroke.Acta cirurgica brasileira · 2023Article
- DL-3-n-butylphthalide alleviates motor disturbance by suppressing ferroptosis in a rat model of Parkinson's disease.Neural regeneration research · 2023Article
- Astragaloside IV attenuate MI-induced myocardial fibrosis and cardiac remodeling by inhibiting ROS/caspase-1/GSDMD signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- Dl-3-n-butylphthalide attenuates myocardial ischemia reperfusion injury by suppressing oxidative stress and regulating cardiac mitophagy via the PINK1/Parkin pathway in rats.Journal of thoracic disease · 2022Article
- Mitochondrial DNA Is a Vital Driving Force in Ischemia-Reperfusion Injury in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- The effect and mechanism of dl-3-n-butylphthalide on angiogenesis in a rat model of chronic myocardial ischemia.American journal of translational research · 2022Article
- Role of Butylphthalide in Immunity and Inflammation: Butylphthalide May Be a Potential Therapy for Anti-Inflammation and Immunoregulation.Oxidative medicine and cellular longevity · 2022Review
- Protective effects of 18β-Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting CaFood science & nutrition · 2021Article
- Dl-3-N-Butylphthalide Presents Anti-Cancer Activity in Lung Cancer by Targeting PD-1/PD-L1 Signaling.Cancer management and research · 2021Article
- Dl-3-n-Butylphthalide Reduces Cognitive Deficits and Alleviates Neuropathology in P301S Tau Transgenic Mice.Frontiers in neuroscience · 2021Article
- Propofol Inhibits Ischemia/Reperfusion-Induced Cardiotoxicity Through the Protein Kinase C/Nuclear Factor Erythroid 2-Related Factor Pathway.Frontiers in pharmacology · 2021Article
- DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial infarction (MI) is an acute and fatal condition that threatens human health. Dl-3-n-butylphthalide (NBP) has been used for the treatment of acute ischemic stroke. Mitochondria may play a protective role in MI injury. However, there are few reports on the cardioprotective effect of NBP or the potential mitochondrial mechanism for the NBP-induced protection against cardiac ischemia injury. We investigated the therapeutic effects of NBP in an in vivo MI model and an in vitro oxidative stress model, as well as the potential mitochondrial mechanism.
methodsThis study comprised two different experiments. The aim of experiment 1 was to determine the protective effects of NBP on MI and the underlying mechanisms in vivo. In part 1, myocardial infarct size was measured by staining with 2,3,5-triphenyltetrazoliumchloride (TTC). Myocardial enzymes and mitochondrial enzymes were assayed. The aim of experiment 2 was to investigate the role of NBP in H
resultsNBP treatment significantly reduced the infarct ratio, as observed by TTC staining, decreased serum myocardial enzymes in MI, and restored heart mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and a-ketoglutarate dehydrogenase (a-KGDH) activities after MI. Moreover, in in vitro studies, NBP significantly increased the viability of H9c2 cells in a dose-dependent manner, reduced cell apoptosis, protected mitochondrial functions, elevated the cellular ATP levels, and promoted H
conclusionCollectively, the results from both the in vivo and in vitro experiments suggested that NBP exerted a cardioprotective effect on cardiac ischemic injury via the regulation of mitochondrial function and biogenesis.
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