摘要
本文用地塞米松（ＤＥＸ）与裸鼠脾细胞共培养，发现ＤＥＸ能有效地诱导脾细胞（包括ＮＫ细胞）发生细胞程序性死亡（ｐｒｏｇｒａｍｍｅｄｃｅｌｌｄｅａｔｈ，ＰＣＤ）或凋亡（ａｐｏｐｔｏｓｉｓ）从而明显抑制脾ＮＫ细胞活性。结果表明：（１）常规电镜显示细胞收缩但胞膜完整，核凝缩，呈现典型的ＰＣＤ特征。（２）加入ＤＥＸ的脾细胞ＤＮＡ琼脂糖凝胶电泳呈现特征性梯状图谱，片段大小为１８０ｂｐ或其倍数，（３）脾ＮＫ细胞活性测定结果表明ＤＥＸ浓度在１０￣（－８）～１０￣（－６）ｍｏｌ／Ｌ范围内可诱导出明显的ＰＣＤ现象发生；而当浓度太低（１０￣（－１０）ｍｏｌ／Ｌ）时则ＰＣＤ现象不明显；当浓度太高（１０￣（－４）ｍｏｌ／Ｌ）时ＰＣＤ现象也不明显，呈现特有的剂量效应关系。（４）动力学结果显示（根据电镜及电泳图）在ＤＥＸ作用１２ｈ已开始有典型的ＰＣＤ现象发生，２４ｈ后则以坏死现象为主。
Dexamethasone(Dex) can effforvely induces apoptosis(or programmed cell death, PCD)in nude mice(NM) spleen cells and inhibits the natural killer oell activity. Our results show that:(1)The chromatin is predomiantly arranged along the nuclear envelope which is entire;(2) Agarose gelelectrophoresis of DNA extracted from NM spleen cells has the typical oligonucleosomal ladder pat-tem ofapoptosis, t3)Dex induas apoptosis ouly when its concentration lies between 10-8 10-6mol/L, (4)Typical apoptosis is induced when the cells were incubated with Dex for 12 hours at37 ℃ ;cell naxosis became predominant after they had been incubated with Dex for 24 hours at37℃ .
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1996年第2期113-116,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
