Expression of S100B Protein in Ischemia/Reperfusion-Induced Brain Injury After Cyclosporine Therapy: A Biochemical Serum Marker with Prognostic Value?
Autor: | Nikolaos Garmpis, Nikolaos Nikiteas, Despina Perrea, Konstantinos Kontzoglou, Christos Dimopoulos, Sotirios Georgopoulos, Afroditi Daskalopoulou, Irini Papaspirou, Christos Damaskos, Marios Papadakis, Stavros Moraitis |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Brain Infarction
Male medicine.medical_specialty medicine.medical_treatment Ischemia S100 Calcium Binding Protein beta Subunit 030204 cardiovascular system & hematology Neuroprotection Brain Ischemia 03 medical and health sciences 0302 clinical medicine medicine.artery Internal medicine Occlusion Medicine Animals Rats Wistar S100b protein Saline business.industry Cerebral infarction Animal Study Brain General Medicine Cerebral Infarction medicine.disease Prognosis Pathophysiology Rats Endocrinology Neuroprotective Agents 030220 oncology & carcinogenesis Reperfusion Injury Brain Injuries Middle cerebral artery Hypoxia-Ischemia Brain Cyclosporine business Biomarkers |
Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
ISSN: | 1643-3750 1234-1010 |
Popis: | BACKGROUND Accumulating evidence has indicated that S100B protein may be involved in the pathophysiology of ischemia-reperfusion brain injury. Cyclosporine has been shown to have neuroprotective functions. This study investigated the effect of cyclosporine on S100B serum levels and the severity of brain tissue damage in a rat model of cerebral ischemia-reperfusion (I/R). MATERIAL AND METHODS Twelve-week-old Wistar male rats were randomly divided into Control I/R and Cyclosporine I/R groups (n=10 each). Cyclosporine was given orally by gavage for 5 days prior to cerebral I/R, at a total volume of 15 mg/kg/day. The Control group received an equal volume of saline. Body weight was measured and all animals were subjected to 60-min focal ischemia by filament occlusion of the middle cerebral artery. ELISA was used to assess the concentrations of serum S100B and development of brain infarct size and neurological outcomes were determined at 2 and 24 h after occlusion withdrawal. RESULTS Cyclosporine improved the neurological deficit score and decreased the cerebral infarct size and body weight. S100B serum levels were significantly elevated in Cyclosporine-treated rats compared with untreated Control rats during the reperfusion phase. Total infarct size was positively associated with S100B serum levels in the Control I/R group, but no significant correlation was observed in the Cyclosporine I/R group. CONCLUSIONS Cyclosporine seems to affect both ischemia-reperfusion brain tissue damage and S100B protein serum levels. S100B serum level appears to be a state marker for the severity of the cerebral ischemia-reperfusion, rather than a trait marker for Cyclosporine responsiveness. |
Databáze: | OpenAIRE |
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