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50只家兔分为内皮剥脱组（BDE，n＝25），药物干预组（BDEP，n＝25），用导管损伤右颈总动脉内皮，左侧为假手术组（S，n＝25）。BDEP组给予三七总皂甙（PNS600mg·kg－1／d）。斑点杂交显影S组未检测出c－myc基因，BDE组术后1h有基因表达，2h达高峰，6h后降至正常。BDEP组与BDE组相比基因表达差异无显著性。3H胸腺嘧啶核苷（3H－TdR）的液闪计数术后36hS组：28±5cpm／μg，BDE组：542±34cpm／μg，BDEP组：56±12cpm／μg；术后76hS组：27±2cpm／μg，BDE组：351±23cpm／μg，BDEP组：30±12cpm／μg。说明PNS对损伤内皮所致的平滑肌增生有抑制作用，其机制不是通过对c－myc基因表达的影响。
Fifty rabbits were divided into two groups: endothelium exfoliative group (BDE, n = 25), drug intervention group (BDEP, n = 25) . BDEP group was given Panax notoginseng saponins (PNS600mg · kg-1 / d). The dot blot hybridization did not detect c-myc gene in S group. The gene expression was observed at 1 hour after operation in BDE group, peaked at 2 hours, and then decreased to normal after 6 hours. There was no significant difference in gene expression between BDEP group and BDE group. 3H-TdR 3H-TdR group: 28 ± 5cpm / μg, BDE group: 542 ± 34cpm / μg, BDEP group: 56 ± 12cpm / μg; 2 cpm / μg, BDE group: 351 ± 23 cpm / μg, BDEP group: 30 ± 12 cpm / μg. PNS on the injured endothelium induced smooth muscle hyperplasia inhibition, the mechanism is not through the c-myc gene expression.