人肺癌变早期阻断及其分子机制研究  

Studies on Inhibition of Human Lung Carcinogenesis in Early Stage by Oltipraz and Its Effects on Some Gene Expression and Regulation

作　　者：柏华[1] 

机构地区：[1]中国协和医科大学中国医学科学院肿瘤研究所

出　　处：《生理科学进展》1998年第3期235-238,共4页Progress in Physiological Sciences

摘　　要：以人胚肺为实验材料，进行了ｏｌｔｉｐｒａｚ对人肺癌变早期阻断及其分子机制的研究。结果显示：ｏｌｔｉｐｒａｚ阻断人肺癌变在香烟凝聚物（ＣＳＣ）运用前或同时运用效果较好；ｏｌｔｉｐｒａｚ阻断人肺癌变时能使谷胱甘肽－Ｓ－转移酶（ＧＳＴｓ）活性和ＧＳＴ－π蛋白含量降低；ｏｌｔｉｐｒａｚ能使ｍｐ５３蛋白表达减弱；ｏｌｔｉｐｒａｚ仅能防止而不能逆转ｒａｓ基因突变；ｏｌｔｉｐｒａｚ能诱导人肺腺癌细胞凋亡，在使用浓度１２０μｇｍｌ效果明显；ＧＳＴ－π的低表达和ｃ－ｆｏｓ的高表达与细胞凋亡相关；By using human fetal lung (HFL) as experimental material, the inhibition of HFL carcinogenesis in early stage by oltipraz and its molecular mechanisms were studied. The results showed that oltipraz is effective in the inhibition of carcinogenesis prior to or at the same time with Cigarette Smoking Condensate(CSC) treatment; oltipraz can decrease GSTs activity and GSTπ protein content along with its inhibition of HFL carcinogenesis; oltipraz can decrease mp53 expression; oltipraz can prevent but can not reverse the ras gene mutation; oltipraz can induce apoptosis of GLC cell obviously in a dosage of 120μgml. Meanwhile, it is related to high expression of cfos and low expression of GSTπ in apoptosis; oltipraz may affect cfos gene expression through induction of a protein factor which links with DSE. 

关 键 词：OLTIPRAZ 基因表达调控 肺癌变 GST-Π 早期阻断 

分 类 号：R734.2[医药卫生—肿瘤]