ArticleMolecular medicine reports2018
Protective effect of polysaccharide peptide on cerebral ischemia‑reperfusion injury in rats.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- LINC01123 aggravates cerebral ischemia reperfusion injury by targeting miR-654-5p to upregulate METTL7A.Scientific reports · 2025Article
- Decoding the Nexus: Cellular and Molecular Mechanisms Linking Stroke and Neurotoxic Microenvironments in Brain Cancer Patients.Biomolecules · 2024Review
- Review
- Targeting inflammation and oxidative stress for protection against ischemic brain injury in rats using cupressuflavone.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Neuroprotective and Anti-inflammatory Effect of Tangeretin Against Cerebral Ischemia-Reperfusion Injury in Rats.Inflammation · 2020Article
- Kaempferol Protects Against Cerebral Ischemia Reperfusion Injury Through Intervening Oxidative and Inflammatory Stress Induced Apoptosis.Frontiers in pharmacology · 2020Article
- Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury.Frontiers in molecular neuroscience · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, the protective effects and regulatory mechanism of polysaccharide peptide (PSP) were investigated in rats with cerebral ischemia‑reperfusion (IR) injury. Neuroblastoma N2a cells were divided into five groups: Negative control; IR injury; PSP low dose treatment; PSP middle dose treatment; and PSP high dose treatment. In vitro, the cell viability was detected by an MTT assay. ELISA was performed to determine the activity of lactate dehydrogenase (LDH) and caspase‑3. A cerebral IR injury model in vivo was established, and hematoxylin and eosin (H&E) staining, western blotting, neurological deficit score and cerebral infarction were assessed. The cell viability was markedly improved following treatment with PSP and the activity of LDH and caspase‑3 was decreased following PSP administration (P<0.05). The in vivo studies determined that the neurological deficit score and cerebral infarction volume were reduced with the concentration of PSP increasing between 150 and 250 mg/kg. The H&E staining indicated that PSP was able to protect the nerve cells against the cerebral IR injury. In addition, PSP upregulated the decreased silent information regulator protein 1, peroxisome proliferator‑-activated receptor γ coactivator‑1α and apoptosis regulator B‑cell lymphoma 2 expression induced by cerebral IR injury. The protein expression level of caspase‑3 and apoptosis regulator apoptosis regulator Bcl‑2‑like protein 4 was downregulated following PSP administration. These results suggested that PSP may improve nerve cell viability, enhance the neuroprotective role in cerebral IR injury and provide a novel approach for the treatment of cerebral IR injury.
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