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Başlık: Sepsis induces apoptotic cell death in different regions of the brain in a rat model of sepsis
Yazarlar: Uludağ Üniversitesi/Tıp Fakültesi/Anatomi Anabilim Dalı.
0000-0003-3368-8123
Kafa, İlker Mustafa
Uysal, Murat
Bakırcı, Sinan
Kurt, Ayberk
AAG-7125-2021
AAR-4341-2020
8450193200
57224848954
24365835600
36615287100
Anahtar kelimeler: Apoptosis
Brain
Caspase-3
Sepsis associated encephalopathy
Tunel
Cerebral-blood-flow
Septic encephalopathy
Laboratory models
Evoked-potentials
Dysfunction
Inflammation
Survival
Shock
Pathophysiology
Mechanisms
Neurosciences & neurology
Yayın Tarihi: 2010
Yayıncı: Nencki Inst Experimental Biology
Atıf: Kafa, İ. M. vd. (2010). "Sepsis induces apoptotic cell death in different regions of the brain in a rat model of sepsis". Acta Neurobiologiae Experimentalis, 70(3), 246-260.
Özet: Sepsis occurs in 14-37% of patients admitted to intensive care units and sepsis associated encephalopathy (SAE) is its severe complication. In an attempt to provide insight into the question how sepsis and SAE contributes cerebral dysfunction, apoptotic cell death was investigated in hippocampal formation, centers of adult neurogenesis and main autonomic centers which are known to regulate heart rate, respiration and other visceral activities, in cecal ligation and puncture (CLP) rat model of sepsis. Vital parameters and electrophysiological changes were monitored for the confirmation of sepsis and SAE, respectively. Apoptotic cell death was evaluated by TUNEL staining, Caspase-3 immunohistochemistry and transmission electron microscope (TEM). Significantly higher number of TUNEL positive apoptotic cells in the median preoptic nucleus, subventricular zone, dentate gyrus and CA1 and CA3 regions of the hippocampal formation were observed in CLP group and Caspase-3 immunohistochemistry and TEM findings were in line with these results, suggesting that the apoptotic cell death would bare a major role in the pathogenesis of the SAE.
URI: https://pubmed.ncbi.nlm.nih.gov/20871644/
http://hdl.handle.net/11452/22490
ISSN: 0065-1400
1689-0035
Koleksiyonlarda Görünür:Scopus
Web of Science

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