摘要
运用体内、体外相结合的方法观察了D-半乳糖(D-gal)对脂质过氧化和蛋白质代谢的影响。结果表明:D-gal使大鼠脑组织、家蝇头和培养大鼠神经细胞、人胚肺二倍体成纤维细胞(HBS)均出现SOD含量下降,MDA和脂褐素(Lipo)水平升高及大鼠全血中谷胱甘肽过氧化物酶(GSH-Px)水平降低等现象;此外,大鼠脑组织中总RNA含量下降,可溶性蛋白减少,不可溶性蛋白增加,这些变化与老年对照相类似,也与黄嘌呤氧化酶-次黄嘌呤系统产生的O2结果一致。提示,在D-gal的代谢过程中伴有活性氧自由基产生,以O2为主的自由基介导的脂质过氧化可能是该脑老化模型的主要原因。
おおhe effects of lipid peroxidation and protein metabolism induced by Dgalactose were investigated in vivo and in vitro.The levels of MDA,lipofuscin,SOD and GSHPx in rat ,house,cultured neruons and human fetal lung fibroblasts were studied respectively.The results showed that the levels MDA and lipofuscin were markedly increased,but SOD and GSHPx decreased,with that the total RNA and dissoluble protein reduced while undissoluble protein was increasde.These reasults were similar to those aged control and HypoxanthineXanthine reaction system(O-2),indicating that reactive oxyger species (ROS) especially (O-2).were generated in the course of Dgalatose metabolism,lipid peroxidation induced by ROS might be the cause of this brain aging model.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
1998年第1期38-40,共3页
Chinese Journal of Gerontology
关键词
D-半乳糖
脂质过氧
脑老化
Brain aging model\ \ Dgalactose\ \ Lipid peroxidation