BACKGROUND:We suggested that the continuous translocation of endotoxin from Gram-negative bacterial overgrowth during bowel rest and total parenteral nutrition (TPN) causes the release of tumor necrosis factor (TNF), resulting in liver damage and hepatic dysfunction. Because TPN-induced hepatic steatosis was significantly reduced by the monoclonal antibodies against TNF, we attempted a more clinically applicable approach using pentoxifylline and thalidomide. METHODS:A control group (group I) fed rat chow and four groups of rats receiving TPN were studied. Group II received TPN only; group III, TPN and 100 mg/kg/d pentoxifylline; group IV, TPN and 200 mg/kg/d pentoxifylline; and group V, TPN and 5 mg/kg/d thalidomide. On day 7, total liver fat was determined. RESULTS:Bowel rest and TPN resulted in a significant (p < .0005) increase in liver fat content that was unaltered by either pentoxifylline or thalidomide. CONCLUSIONS:Our results show no role for pentoxifylline or thalidomide in reducing TPN-associated hepatic steatosis.

译文

背景:我们建议肠道休息和全胃肠外营养(TPN)期间革兰氏阴性细菌过度生长引起的内毒素的连续移位会导致肿瘤坏死因子(TNF)的释放,从而导致肝损伤和肝功能障碍。由于针对TNF的单克隆抗体可显着降低TPN诱导的肝脂肪变性,因此我们尝试使用己酮可可碱和沙利度胺进行临床治疗。
方法:对对照组(I组)喂食大鼠食物和四组接受TPN的大鼠进行研究。第二组仅收到TPN; III组,TPN和100 mg / kg / d己酮可可碱; IV组,TPN和200 mg / kg / d己酮可可碱; V组,TPN和5 mg / kg / d沙利度胺。在第7天,测定总肝脂肪。
结果:大便休息和TPN导致肝脂肪含量显着增加(p <.0005),而己酮可可碱或沙利度胺均未改变。
结论:我们的结果显示己酮可可碱或沙利度胺在减少TPN相关性肝脂肪变性中没有作用。

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