摘要
目的 :耗竭肝脏还原型谷胱甘肽 (GSH)导致氧化还原失平衡后 ,肝脏枯否细胞的吞噬功能发生何种变化从而影响半乳糖胺 /脂多糖 (Galn/LPS)介导的肝损伤。方法 :对雄性昆明种小鼠注射Galn/LPS造成急性肝损伤 ,实验组在给予Galn/LPS前腹腔注射马来酸二乙酯 (DEM)。结果 :体内、体外实验结果显示 ,单纯DEM注射 1 .5h或 6h ,对枯否细胞吞噬功能无明显影响 ;Galn/LPS注射 1 .5h、6h后 ,肝损伤组枯否细胞吞噬指数显著高于其它各组 ;DEM预处理则可明显降低Galn/LPS所致枯否细胞吞噬指数的升高。结论 :一方面活化的枯否细胞参与Galn/LPS所致肝损伤发生 ,另一方面也表明DEM减轻Galn/LPS诱发肝损伤与其抑制LPS所致枯否细胞活化有关。
Objective:In case of exhausting the hepatic glutathione(GSH) to cause a redox disequilirium,what changement happened on kupffer cell's(KC) phagocytosis,so as to influence tle occurrence of liver injure.Method:Diethylmaleate(DEM) was injected to mice to exhaust their GSH.Results:After treated with DEMbefore the Galn/LPS injuction,can deduce the increased of KC's index which caused by Galn/LPS.Conclusion:DEM can depete GSH in liver and modulate redox balance to inhibit liver injury induced by Galn/LPS.
出处
《长治医学院学报》
2004年第2期86-88,共3页
Journal of Changzhi Medical College
