Acute Brain Inflammation and Oxidative Damage Are Related to Long-Term Cognitive Deficits and Markers of Neurodegeneration in Sepsis-Survivor Rats
العنوان: | Acute Brain Inflammation and Oxidative Damage Are Related to Long-Term Cognitive Deficits and Markers of Neurodegeneration in Sepsis-Survivor Rats |
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المؤلفون: | Cristiane Ritter, Francieli Vuolo, Fabricia Petronilho, José Cláudio Fonseca Moreira, Clarissa M. Comim, Mágada Tessmann Schwalm, João Quevedo, João Paulo Almeida dos Santos, Felipe Dal-Pizzol, Daniel Pens Gelain, Matheus Augusto de Bittencourt Pasquali, Samantha Pereira Miguel |
المصدر: | Molecular Neurobiology. 49:380-385 |
بيانات النشر: | Springer Science and Business Media LLC, 2013. |
سنة النشر: | 2013 |
مصطلحات موضوعية: | Male, medicine.medical_specialty, Time Factors, Synaptophysin, Neuroscience (miscellaneous), Hippocampus, Inflammation, medicine.disease_cause, Sepsis, Cellular and Molecular Neuroscience, Internal medicine, medicine, Animals, Survivors, Rats, Wistar, Prefrontal cortex, Cognitive deficit, Amyloid beta-Peptides, biology, Neurodegeneration, Neurodegenerative Diseases, medicine.disease, Rats, Oxidative Stress, Endocrinology, nervous system, Neurology, Acute Disease, biology.protein, Encephalitis, medicine.symptom, Cognition Disorders, Psychology, Neuroscience, Biomarkers, Oxidative stress |
الوصف: | Survivors from sepsis present long-term cognitive deficits and some of these alterations resemble the pathophysiological mechanisms of neurodegenerative diseases. For this reason, we analyzed beta-amyloid peptide (Aβ) and synaptophysin levels in the brain of rats that survived from sepsis and their relation to cognitive dysfunction and to acute brain inflammation. Sepsis was induced in rats by cecal ligation and puncture, and 30 days after surgery, the hippocampus and prefrontal cortex were isolated just after cognitive evaluation by the inhibitory avoidance test. The immunocontent of Aβ and synaptophysin were analyzed by Western blot analysis. Aβ increased and synaptophysin decreased in septic animals both in the hippocampus and prefrontal cortex concurrent with the presence of cognitive deficits. Prefrontal levels of synaptophysin correlated to the performance in the inhibitory avoidance. Two different treatments known to decrease brain inflammation and oxidative stress when administered at the acute phase of sepsis decreased Aβ levels both in the prefrontal cortex and hippocampus, increased synaptophysin levels only in the prefrontal cortex, and improved cognitive deficit in sepsis-survivor animals. In conclusion, we demonstrated that brain from sepsis-survivor animals presented an increase in Aβ content and a decrease in synaptophysin levels and cognitive impairment. These alterations can be prevented by treatments aimed to decrease acute brain inflammation and oxidative stress. |
تدمد: | 1559-1182 0893-7648 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9b28fdeccc0ba557298d42ad06a5638f https://doi.org/10.1007/s12035-013-8526-3 |
حقوق: | CLOSED |
رقم الأكسشن: | edsair.doi.dedup.....9b28fdeccc0ba557298d42ad06a5638f |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15591182 08937648 |
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