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首页> 外文期刊>The Journal of Nutritional Biochemistry >Protein-energy malnutrition increases activation of the transcription factor, nuclear factor kappaB, in the gerbil hippocampus following global ischemia.
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Protein-energy malnutrition increases activation of the transcription factor, nuclear factor kappaB, in the gerbil hippocampus following global ischemia.

机译：蛋白质能量营养不良会增加全球缺血后沙鼠海马中转录因子核因子κB的活化。

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摘要

Protein-energy malnutrition (PEM) exacerbates functional impairment caused by brain ischemia. This is correlated with reactive gliosis, which suggests an increased inflammatory response. The objective of the current study was to investigate if PEM increases hippocampal activation of nuclear factor kappaB (NFkappaB), a transcription factor that amplifies the inflammatory response involved in ischemic brain injury. Mongolian gerbils (11-12 weeks old) were randomly assigned to control diet (12.5% protein) or protein-deficient diet (2%) for 4 weeks. The 2% protein group had a 15% decrease in voluntary food intake (P<.001; unpaired t test), resulting in PEM. Body weight after 4 weeks was 20% lower in the PEM group (P<.001). Gerbils were then exposed to sham surgery or global ischemia induced by 5-min bilateral common carotid artery occlusion. PEM independently increased hippocampal NFkappaB activation detected by electrophoretic mobility shift assay at 6 h after surgery (P=.014; 2-factor ANOVA). Ischemia did not significantly affect NFkappaB activation nor was there interaction between diet and ischemia. Serum glucose and cortisol concentrations at 6 h postischemia were unaltered by diet or ischemia. A second experiment using gerbils of the same age and feeding paradigm demonstrated that PEM also increases hippocampal NFkappaB activation in the absence of surgery. These findings suggest that PEM, which exists in 16% of elderly patients at admission for stroke, may worsen outcome by increasing activation of NFkappaB. Since PEM increased NFkappaB activation independent of ischemia or surgery, the data also have implications for the inflammatory response of the many individuals affected globally by PEM.
机译：蛋白质能量营养不良（PEM）加剧了由脑缺血引起的功能损害。这与反应性神经胶质增生相关，这表明炎症反应增加。当前研究的目的是研究PEM是否增加海马核因子kappaB（NFkappaB）的激活，NFkappaB是一种转录因子，可放大与缺血性脑损伤有关的炎症反应。蒙古沙鼠（11-12周龄）被随机分配为对照饮食（蛋白质含量为12.5％）或蛋白质缺乏饮食（含量为2％），持续4周。 2％蛋白质组的自愿食物摄入量减少了15％（P <.001;未配对t检验），导致PEM。 PEM组4周后的体重降低了20％（P <.001）。然后将沙鼠暴露于由5分钟的双侧颈总动脉闭塞引起的假手术或整体缺血。 PEM在手术后6小时通过电泳迁移率迁移分析独立检测到增加了海马NFkappaB激活（P = .014; 2因子ANOVA）。缺血并不显着影响NFκB的活化，饮食与缺血之间也没有相互作用。饮食或缺血后，缺血后6 h的血清葡萄糖和皮质醇浓度未改变。使用相同年龄和进食模式的沙鼠进行的第二项实验表明，PEM在无需手术的情况下也可提高海马NFkappaB的激活。这些发现表明，PEM在中风住院时占16％的老年患者中，其可能通过增加NFkappaB的激活而使预后恶化。由于PEM增加了NFkappaB的激活，而不受缺血或手术的影响，因此该数据也对受PEM影响的许多个体的炎症反应具有影响。

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