摘要
采用内皮素－１（ＥＴ－１０．１μｍｏｌ·Ｌ－１）建立培养的血管平滑肌细胞增殖模型，用［３Ｈ］胸腺嘧啶核苷（［３Ｈ］ＴｄＲ）参入法，流式细胞术，免疫细胞化学及Ｎｏｒｔｈｅｒｎｂｌｏｔ方法，观察了１－（２，６－二甲基苯氧基）－２－（３，４－二甲氧基苯乙氨基）丙烷盐酸盐（ＤＤＰＨ０．１μｍｏｌ·Ｌ－１）对血管平滑肌细胞增殖的作用及对原癌基因及抑癌基因的影响．结果发现：ＤＤＰＨ能逆转ＥＴ－１所致［３Ｈ］ＴｄＲ参入量增多，阻止血管平滑肌细胞由静止期（Ｇ０／Ｇ１期）进入ＤＮＡ合成期（Ｓ期）和有丝分裂期（Ｇ２／Ｍ期），并能逆转ＥＴ－１引起的ｃ－ｆｏｓ，ｃ－ｍｙｃ，ｃ－ｓｉｓ原癌基因相关抗原及ｍＲＮＡ表达增强，Ｐ５３抑癌基因相关抗原及ｍＲＮＡ表达减弱．提示ＤＤＰＨ能抑制血管平滑肌细胞增殖，与癌基因调控的分子生物学机理有关．
In order to determine the effects of 1 (2,6 dimethylphenoxy) 2 (3,4 dimethoxy phenylethylamino) propane hydrochloride (DDPH 0.1 μmol·L 1 ) on endothelin 1 (ET 1 0.1 μmol·L 1 ) stimulated proliferation of vascular smooth muscle cells (VSMC) and expression of oncogene c myc, c fos, c sis, and antioncogene P53, the experimental models of proliferation of cultured porcine aortic smooth muscle cells induced by ET 1 were established, and thymidine ( TdR) incorporation, flow cytometry, immunohistochem istry and Northern blot assays were used. The results showed that DDPH may drop TdR data increased by ET 1 and hold back VSMC from static phase (G 0/G 1) to DNA synthetic phase (S) and mitotic phase (G 2/M). Furthermore, DDPH could reverse the enhanced expression of oncogene c myc, c fos, c sis and reduced expression of antioncogene P53 induced by ET 1. These results suggest that DDPH may inhibit DNA synthesis and proliferation of VSMC, related with the mechanism of molecular biology of controlling oncogene.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1997年第3期187-189,共3页
Chinese Journal of Pharmacology and Toxicology
基金
国家卫生部科研基金
关键词
降压剂
丙烷盐酸盐
内皮素
原癌基因
血管平滑肌
antihypertensive agents
1 (2
6 dimethylphenoxy) 2 (3
4 dimethoxyphenylethy lamino) propane hydrochloride
endothelins
muscle
smooth
vascular
proto oncogene
