Neuroprotective effect of chondroitinase ABC on primary and secondary brain injury after stroke in hypertensive rats
Abstract
Focal cerebral infarction causes secondary damage in the ipsilateral ventroposterior thalamic nucleus (VPN). Chondroitin sulfate proteoglycans (CSPGs) are a family of putative inhibitory components, and its degradation by chondroitinase ABC (ChABC) promotes post-injury neurogenesis. This study investigated the role of ChABC in the primary and secondary injury post stroke in hypertension. Renovascular hypertensive Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO), and were subjected to continuous intra-infarct infusion of ChABC (0.12 U/d for 7 days) 24 h later. Neurological function was evaluated by a modified neurologic severity score. Neurons were counted in the peri-infarct region and the ipsilateral VPN 8 and 14 days after MCAO by Nissl staining and NeuN labeling. The expressions of CSPGs, growth-associated protein-43 (GAP-43) and synaptophysin (SYN) were detected with immunofluorescence or Western blotting. The intra-infarct infusion of ChABC, by degrading accumulated CSPGs, rescued neuronal loss and increased the levels of GAP-43 and SYN in both the ipsilateral cortex and VPN, indicating enhancd neuron survival as well as augmented axonal growth and synaptic plasticity, eventually improving overall neurological function. The study demonstrated that intra-infarct ChABC infusion could salvage the brain from both primary and secondary injury by the intervention on the neuroinhibitory environment post focal cerebral infarction.
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After thalamic stroke in hypertensive rats, continuous intra-infarct infusion of ChABC enhanced levels of synaptophysin and growth-associated protein 43.
“After thalamic stroke in hypertensive rats, the continuous intra-infarct infusion of ChABC rescued neuronal loss and enhanced levels of synaptophysin and growth-associated protein 43 indicating augmented axonal growth as well as synaptic plasticity to finally ensure overall neuronal function (Chen et al., 2014).”
From Damaged Neocortical Perineuronal Nets Due to Experimental Focal Cerebral Ischemia in Mice, Rats and Sheep (2017) · cites this paper as Chen et al., 2014
After thalamic stroke in hypertensive rats, continuous intra-infarct infusion of ChABC ensured overall neuronal function.
“After thalamic stroke in hypertensive rats, the continuous intra-infarct infusion of ChABC rescued neuronal loss and enhanced levels of synaptophysin and growth-associated protein 43 indicating augmented axonal growth as well as synaptic plasticity to finally ensure overall neuronal function (Chen et al., 2014).”
From Damaged Neocortical Perineuronal Nets Due to Experimental Focal Cerebral Ischemia in Mice, Rats and Sheep (2017) · cites this paper as Chen et al., 2014
After thalamic stroke in hypertensive rats, continuous intra-infarct infusion of ChABC rescued neuronal loss.
“After thalamic stroke in hypertensive rats, the continuous intra-infarct infusion of ChABC rescued neuronal loss and enhanced levels of synaptophysin and growth-associated protein 43 indicating augmented axonal growth as well as synaptic plasticity to finally ensure overall neuronal function (Chen et al., 2014).”
From Damaged Neocortical Perineuronal Nets Due to Experimental Focal Cerebral Ischemia in Mice, Rats and Sheep (2017) · cites this paper as Chen et al., 2014
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- Authors
- Chen, X.-R., Liao, S.-J., Ye, L.-X., Gong, Q., Ding, Q., Zeng, J.-S., & Yu, J.
- Affiliations
- Sun Yat-sen University (CN)
- Guangdong Provincial People's Hospital (CN)
- Corresponding author
- Yu, Jian
- ORCID
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 1543
- Pages
- 324-333
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W1982539946
- Cited by
- 43
- References
- 48
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 5 · 2015: 6 · 2014: 2
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81371276)
- Youth Teacher Training Project of Basic Scientific Research Grant of Sun Yat-sen University, Chin (09ykpy48)
- Youth Project of National Natural Science Foundation of China (81100871)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- chondroitinase ABC, chondroitin sulfate proteoglycans, secondary brain injury, stroke, hypertension, middle cerebral artery occlusion, ventroposterior thalamic nucleus, neuroprotection, axon growth, synaptic plasticity, neuronal survival, GAP-43, synaptophysin
- MeSH terms
- Analysis of Variance, Animals, Brain Injuries, Cell Count, Disease Models, Animal, Hypertension, Functional Laterality, Male, Neurologic Examination, Phosphopyruvate Hydratase, Chondroitin Sulfate Proteoglycans, Time Factors, Rats, Sprague-Dawley, Neuroprotective Agents, Chondroitin ABC Lyase, GAP-43 Protein, Infarction, Middle Cerebral Artery, Brain Infarction, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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