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为探讨API0134防治冠状动脉粥样硬化和腔内成形术后再狭窄的作用机制，采用内皮素诱导建立培养的血管平滑肌细胞增殖模型，用氚标胸腺嘧啶脱氧核苷掺入法、流式细胞术、免疫细胞化学检测及Northernblot方法，观察了API0134对血管平滑肌细胞增殖的作用及对血小板源生长因子B链、碱性纤维母细胞生长因子及其相关癌基因C－sis和C－mpc表达的影响。结果发现，API0134能逆转内皮素所致的氚标胸腺嘧啶脱氧核苷掺入量增多（对照组为499±92，内皮素组为617±98，API0134组为506±102），阻止血管平滑肌细胞由静止期（G0／G1期；对照组为72％，内皮素组为50％，API0134组为60％）进入DNA合成期（S期；三组分别为26％、36％和30％）和有丝分裂期（G2／M期，三组分别为2％、14％和4％），并能逆转内皮素引起的血小板源生长因子B链、碱性纤维母细胞生长因子抗原、c－sis和c－mpc的mRNA表达增强。提示API0134有抑制血管平滑肌细胞增殖的作用，这种作用与生长因子及癌基因调控的分子生物学机制有关。
To explore the mechanism of action of API0134 in preventing and treating coronary atherosclerosis and restenosis after endoluminoplasty, the model of vascular smooth muscle cell proliferation induced by endothelin was established. Tritiated thymidine incorporation, flow cytometry , Immunocytochemistry and Northern blotting method were used to observe the effect of API0134 on the proliferation of vascular smooth muscle cells and the effect on the expression of platelet-derived growth factor B chain, basic fibroblast growth factor and its related oncogene C-sis and C-mpc . The results showed that API0134 could reverse the increase of endotoxin-induced tritium thymidine incorporation (499 ± 92 in the control group, 617 ± 98 in the endothelin group, and 506 ± 102 in the API0134 group), preventing vascular smooth muscle cells The DNA synthesis phase (S phase; 26%, 36%, and 30%, respectively) entered the quiescent phase (G0 / G1 phase; 72% in the control group, 50% in the endothelin group and 60% in the API0134 group) Mitosis (G2 / M phase, 2%, 14%, and 4%, respectively) in the three groups, and reverses endothelin-induced platelet derived growth factor B chain, basic fibroblast growth factor antigens, c-sis and c MRNA expression of -mpc is enhanced. Suggesting that API0134 can inhibit the proliferation of vascular smooth muscle cells. This effect is related to the molecular mechanism of growth factors and oncogenes regulation.