Solulin reduces infarct volume and regulates gene-expression in transient middle cerebral artery occlusion in rats
Open accessAbstract
BACKGROUND: Thrombolysis after acute ischemic stroke has only proven to be beneficial in a subset of patients. The soluble recombinant analogue of human thrombomodulin, Solulin, was studied in an in vivo rat model of acute ischemic stroke. METHODS: Male SD rats were subjected to 2 hrs of transient middle cerebral artery occlusion (tMCAO). Rats treated with Solulin intravenously shortly before reperfusion were compared to rats receiving normal saline i.v. with respect to infarct volumes, neurological deficits and mortality. Gene expression of IL-6, IL-1β, TNF-α, MMP-9, CD11B and GFAP were semiquantitatively analyzed by rtPCR of the penumbra. RESULTS: 24 hrs after reperfusion, rats were neurologically tested, euthanized and infarct volumes determined. Solulin significantly reduced mean total (p=0.001), cortical (p=0.002), and basal ganglia (p=0.036) infarct volumes. Hippocampal infarct volumes (p=0.191) were not significantly affected. Solulin significantly downregulated the expression of IL-1β (79%; p<0.001), TNF-α (59%; p=0.001), IL-6 (47%; p=0.04), and CD11B (49%; p=0.001) in the infarcted cortex compared to controls. CONCLUSIONS: Solulin reduced mean total, cortical and basal ganglia infarct volumes and regulated a subset of cytokines and proteases after tMCAO suggesting the potency of this compound for therapeutic interventions.
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The tMCAO model reflects events that occur in ischaemic stroke in humans after treatment with thrombolytic agents.
“This model reflects events that occur in ischaemic stroke in humans after treatment with thrombolytic agents [28,29].”
From Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats (2020) · cites this paper as [29]
The Methods (page unavailable) describe a rat tMCAO model in which blood flow was restored by removing the occluding thread. The Background (page unavailable) discusses thrombolytic treatment in human stroke, but the paper does not state that thread-removal reperfusion reflects events after thrombolysis in humans. (LLM, conf=0.78)
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- Authors
- Ryang, Y.-M., Dang, J., Kipp, M., Petersen, K.-U., Fahlenkamp, A. V., Gempt, J., Wesp, D., Rossaint, R., Beyer, C., & Coburn, M.
- Affiliations
- TUM Klinikum (DE)
- RWTH Aachen University (DE)
- Paion (Germany) (DE)
- Universitätsklinikum Aachen (DE)
- Universitätsmedizin Göttingen (DE)
- Corresponding author
- Ryang, Yu-Mi
- Venue
- BMC Neuroscience
- Published
- 2011-11-14
- Volume
- 12
- Issue
- 1
- Pages
- 113-113
- ISSN
- 1471-2202 (ISSN-L)
- PMC
- PMC3251036
- OpenAlex
- W1998528194
- Cited by
- 30
- References
- 40
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 6 · 2014: 3 · 2013: 3 · 2012: 3
- FWCI
- 2.17
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- BMC Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion, cc-by)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- GRO (submittedVersion, cc-by)
- RWTH Publications (RWTH Aachen) (submittedVersion, cc-by)
- RWTH Publications (RWTH Aachen)
- Funders
- RWTH Aachen University
- Topics
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- thrombomodulin, acute ischemic stroke, transient middle cerebral artery occlusion, infarct size, neuroinflammation, cytokines, IL-1β, TNF-α, interleukin-6, CD11b, MMP-9, glial fibrillary acidic protein, penumbra, reperfusion, basal ganglia infarction, neuroprotection
- MeSH terms
- Animals, Ischemic Attack, Transient, Disease Models, Animal, Gene Expression Regulation, Male, Recombinant Proteins, Rats, Sprague-Dawley, Receptors, Thrombin, Neuroprotective Agents, Infarction, Middle Cerebral Artery, Brain Infarction, Rats
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