ArticleJournal of neuroinflammation2018
Cell permeable HMGB1-binding heptamer peptide ameliorates neurovascular complications associated with thrombolytic therapy in rats with transient ischemic stroke.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Imbalanced VWF-ADAMTS13 axis contributes to the detrimental impact of a preceding respiratory tract infection on stroke.Blood advances · 2025Article
- Crosstalk Among Glial Cells in the Blood-Brain Barrier Injury After Ischemic Stroke.Molecular neurobiology · 2024Review
- Immune regulation of the gut-brain axis and lung-brain axis involved in ischemic stroke.Neural regeneration research · 2024Review
- Apolipoprotein E mimetic peptide COG1410 alleviates blood‑brain barrier injury in a rat model of ischemic stroke.Molecular medicine reports · 2023Article
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
- Modulation of α7nAchR by Melatonin Alleviates Ischemia and Reperfusion-Compromised Integrity of Blood-Brain Barrier Through Inhibiting HMGB1-Mediated Microglia Activation and CRTC1-Mediated Neuronal Loss.Cellular and molecular neurobiology · 2022Article
- Inflammatory Responses After Ischemic Stroke.Seminars in immunopathology · 2022Review
- Flufenamic acid improves survival and neurologic outcome after successful cardiopulmonary resuscitation in mice.Journal of neuroinflammation · 2022Article
- Roles of Nitric Oxide in Brain Ischemia and Reperfusion.International journal of molecular sciences · 2022Review
- Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment in Acute Ischemic Stroke.Cellular and molecular neurobiology · 2022Review
- Verapamil as an Adjunct Therapy to Reduce tPA Toxicity in Hyperglycemic Stroke: Implication of TXNIP/NLRP3 Inflammasome.Molecular neurobiology · 2021Article
- Class IIa HDAC Downregulation Contributes to Surgery-Induced Cognitive Impairment Through HMGB1-Mediated Inflammatory Response in the Hippocampi of Aged Mice.Journal of inflammation research · 2021Article
- Glycyrrhizin Prevents Hemorrhagic Transformation and Improves Neurological Outcome in Ischemic Stroke with Delayed Thrombolysis Through Targeting Peroxynitrite-Mediated HMGB1 Signaling.Translational stroke research · 2020Article
- Tissue Plasminogen Activator Promotes TXNIP-NLRP3 Inflammasome Activation after Hyperglycemic Stroke in Mice.Molecular neurobiology · 2020Article
- The Protective Role of Immunomodulators on Tissue-Type Plasminogen Activator-Induced Hemorrhagic Transformation in Experimental Stroke: A Systematic Review and Meta-Analysis.Frontiers in pharmacology · 2020Article
- The Roles of High Mobility Group Box 1 in Cerebral Ischemic Injury.Frontiers in cellular neuroscience · 2020Review
- Article
- Clinical significance of high-mobility group box-1 (HMGB1) in subjects with type 2 diabetes mellitus (T2DM) combined with chronic obstructive pulmonary disease (COPD).Journal of clinical laboratory analysis · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundBlood-brain barrier (BBB) breakdown and inflammatory responses are the major causes of tissue-type plasminogen activator (tPA)-induced hemorrhagic transformation (HT), while high-mobility group box 1 (HMGB1) exacerbates inflammatory damage to BBB during the process of brain ischemia/reperfusion. This study aimed to investigate the change of HMGB1 after thrombolytic therapy and whether blocking HMGB1 could ameliorate the neurovasculature complications secondary to tPA treatment in stroke rats.
methodsSera from acute stroke patients and rats with thrombolytic therapy were collected to investigate HMGB1 secretion. Male Sprague-Dawley rats with 2 h or 4.5 h middle cerebral artery occlusion were continuously infused with tPA followed by administration of membrane permeable HMGB1-binding heptamer peptide (HBHP). The mortality rate, neurological score, HT, brain swelling, BBB permeability, and inflammatory factors were determined.
resultsThe results revealed that HMGB1 levels were elevated in both stroke patients and rats after tPA treatment. Blocking HMGB1 signaling by HBHP in the rat model of 4.5 h brain ischemia significantly attenuated tPA-related complications, including mortality rate, the degree of hemorrhage, brain swelling, neurological deficits, BBB impairment, microglia activation, and the expressions of inflammatory cytokines.
conclusionstPA treatment might induce HMGB1 secretion while blocking HMGB1 with HBHP could markedly reduce the risk of thrombolysis-associated brain hemorrhage and mortality through attenuating BBB damage and inflammatory reactions. These results indicate that HMGB1 may potentiate the risk of HT in tPA administration and that blocking HMGB1 signaling would be helpful in preventing complications brought by thrombolysis in ischemic stroke.
trial registrationhttp://www.chictr.org.cn . Unique identifier: ChiCTR-OOC-16010052. Registered 30 November 2016.
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