ArticleTranslational stroke research2018
Baicalin Attenuates Blood-Brain Barrier Disruption and Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke Rats with Delayed t-PA Treatment: Involvement of ONOO
Article in Translational stroke research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 110 citations in OpenAlex.
- Baicalin and CNS-related diseases: new insights into neuroprotective potentials based on underlying mechanisms.Biochemistry and biophysics reports · 2026Review
- Ischemic stroke: molecular mechanisms of blood-brain barrier dysfunction and opportunities for drug development.Fluids and barriers of the CNS · 2026Review
- Pachymic Acid Targets PI3K/Akt Signaling Pathway to Attenuate tPA-Induced Hemorrhagic Transformation After Ischemic Stroke.CNS neuroscience & therapeutics · 2026Article
- Ischemic stroke and intervention strategies based on the timeline of stroke progression: Review and prospects.Acta pharmaceutica Sinica. B · 2025Review
- Review
- Effects of a mitochondrial calcium uniporter and P-selectin inhibitors on neural injury induced by global cerebral ischemia-reperfusion in male rats.Metabolic brain disease · 2025Article
- Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms.Heliyon · 2025Review
- Acupuncture alleviates hemorrhagic transformation after delayed rt-PA treatment for acute ischemic stroke by regulating the mitophagy-NLRP3 inflammasome pathway.Frontiers in neurology · 2025Article
- Polyphenolic metabolites inFrontiers in pharmacology · 2025Review
- Peroxynitrite-Triggered Carbon Monoxide Donor Improves Ischemic Stroke Outcome by Inhibiting Neuronal Apoptosis and Ferroptosis.Molecular neurobiology · 2024Article
- Neural repair function of osteopontin in stroke and stroke‑related diseases (Review).Experimental and therapeutic medicine · 2024Review
- Hypochlorous acid derived from microglial myeloperoxidase could mediate high-mobility group box 1 release from neurons to amplify brain damage in cerebral ischemia-reperfusion injury.Journal of neuroinflammation · 2024Article
- Biomimetic nanoparticles in ischemic stroke therapy.Discover nano · 2023Review
- Ancient Chinese Herbal Recipe Huanglian Jie Du Decoction for Ischemic Stroke: An Overview of Current Evidence.Aging and disease · 2022Article
- Angong Niuhuang Wan reduces hemorrhagic transformation and mortality in ischemic stroke rats with delayed thrombolysis: involvement of peroxynitrite-mediated MMP-9 activation.Chinese medicine · 2022Article
- Roles of Nitric Oxide in Brain Ischemia and Reperfusion.International journal of molecular sciences · 2022Review
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Elucidating the Synergistic Effect of Multiple Chinese Herbal Prescriptions in the Treatment of Post-stroke Neurological Damage.Frontiers in pharmacology · 2022Article
- The Putative Role of Astaxanthin in Neuroinflammation Modulation: Mechanisms and Therapeutic Potential.Frontiers in pharmacology · 2022Review
- Neurovascular Units and Neural-Glia Networks in Intracerebral Hemorrhage: from Mechanisms to Translation.Translational stroke research · 2021Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
Tissue plasminogen activator (t-PA) has a restrictive therapeutic window within 4.5 h after ischemic stroke with the risk of hemorrhagic transformation (HT) and neurotoxicity when it is used beyond the time window. In the present study, we tested the hypothesis that baicalin, an active compound of medicinal plant, could attenuate HT in cerebral ischemia stroke with delayed t-PA treatment. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 4.5 h and then continuously received t-PA infusion (10 mg/kg) for 0.5 h and followed by 19-h reperfusion. Baicalin (50, 100, 150 mg/kg) was administrated via femoral vein at 4.5 h after MCAO cerebral ischemia. Delayed t-PA infusion significantly increased the mortality rate, induced HT, blood-brain barrier (BBB) damage, and apoptotic cell death in the ischemic brains and exacerbated neurological outcomes in cerebral ischemia-reperfusion rats at 24 h after MCAO cerebral ischemia. Co-treatment of baicalin significantly reduced the mortality rates, ameliorated the t-PA-mediated BBB disruption and HT. Furthermore, baicalin showed to directly scavenge peroxynitrite and inhibit MMP-9 expression and activity in the ischemic brains with the delayed t-PA treatment. Baicalin had no effect on the t-PA fibrinolytic function indicated by t-PA activity assay. Taken together, baicalin could attenuate t-PA-mediated HT and improve the outcomes of ischemic stroke treatment possibly via inhibiting peroxynitrite-mediated MMP-9 activation.
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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.