Kafa Ilker M, Uysal Murat, Bakirci Sinan, Ayberk Kurt M
Uludag University, Faculty of Medicine, Anatomy Department, Bursa, Turkey.
Acta Neurobiol Exp (Wars). 2010;70(3):246-60. doi: 10.55782/ane-2010-1796.
Sepsis occurs in 14-37 percent 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.
脓毒症发生在14%至37%入住重症监护病房的患者中，脓毒症相关脑病（SAE）是其严重并发症。为了深入了解脓毒症和SAE如何导致脑功能障碍，在盲肠结扎和穿刺（CLP）脓毒症大鼠模型中，对海马结构、成年神经发生中心以及已知调节心率、呼吸和其他内脏活动的主要自主神经中心的凋亡细胞死亡情况进行了研究。分别监测生命体征参数和电生理变化以确认脓毒症和SAE。通过TUNEL染色、Caspase-3免疫组织化学和透射电子显微镜（TEM）评估凋亡细胞死亡情况。在CLP组中，观察到视前正中核、脑室下区、齿状回以及海马结构的CA1和CA3区域中TUNEL阳性凋亡细胞数量显著增加，Caspase-3免疫组织化学和TEM结果与这些结果一致，表明凋亡细胞死亡在SAE的发病机制中起主要作用。
