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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．
Cultured vascular smooth muscle cell proliferation models were established using endothelin-1 (ET-10.1μmol·L-1). Flow cytometry and immunocytochemistry were performed using [3H] thymidine incorporation, And Northern blot method were used to observe the effect of 1- (2,6-dimethylphenoxy) -2- (3,4-dimethoxyphenethylamino) propane hydrochloride (DDPH 0.1 μmol·L -1) Vascular Smooth Muscle Cell Proliferation and Its Effects on Proto - oncogenes and Tumor Suppressor Genes. The results showed that DDPH could reverse the increase of the [3H] TdR incorporation caused by ET-1 and prevent the smooth muscle cells from entering the DNA synthesis phase (S phase) and the mitotic phase (G2 / M phase) from quiescent phase (G0 / G1 phase) And could reverse the expression of c-fos, c-myc, c-sis proto-oncogene related antigens and mRNAs induced by ET-1, and the expression of anti-oncogene related antigens and mRNA of P53 was weakened. Tip DDPH can inhibit the proliferation of vascular smooth muscle cells, and oncogene regulation of molecular biology.