中文摘要：

目的研究芎芍胶囊对实验性兔动脉粥样硬化（AS）血管平滑肌细胞（VSMC）凋亡的影响，并探讨其可能的机制。方法采用4F·Fogarty导管剥脱损伤腹主动脉内皮后继喂高脂饲料的方法，复制兔节段性AS模型。术后随机分为8组，即模型3d组、2周组、6周组，单纯内皮损伤组，普罗布考组，芎芍胶囊小剂量组、大剂量组及正常对照组。除正常对照组及单纯内皮损伤组外均予高脂饲料喂养，采用TUNEL法检测新生内膜中平滑肌细胞（SMC）的凋亡情况，采用放射免疫法测定血浆血管紧张素l（Angl）的水平，观察药物对其的影响。结果内皮损伤喂食高脂饲料3d，血浆AngⅡ水平逐渐升高，6周时与正常对照组比较有统计学意义（P〈0．01），芎芍大剂量组明显降低血浆AngⅡ水平，与模型6周组比较有统计学意义（P〈0．05），普罗布考组及芎芍小剂量组亦有降低AngⅡ水平的趋势，但无统计学意义。TUNEL染色结果显示，模型3d已出现凋亡细胞，2周及6周时细胞凋亡进一步增多，芎芍胶囊大、小剂量组凋亡细胞阳性表达率均高于模型6周组，普罗布考组凋亡细胞阳性表达率与模型6周组比较有升高趋势，但无统计学意史。结论芎芍胶囊可明显降低血浆AngⅡ水平，促进SMC凋亡，从而抑制AS的发生发展。

英文摘要：

Objective To study effects of Xiongshao Capsule （XSC） on apoptosis of vascular smooth muscle cells （SMC） in rabbits with experimental atherosclerosis （AS）, and to explore its possible mechanisms. Methods Rabbit＇s fractional AS model was established by denuding and injuring of endodermis in abdominal artery with 4F. Fogarty catheter, and followed with high cholesterol feeding. The animals were randomly divided into 8 groups： Model group A, B and C （following balloon injury for 3 days, 2 weeks and 6 weeks, respectively）, the low - dose XSC group （F） and high - dose XSC group （G）, normal control group （N）, single endothelium injury group （D）, and probucol group （E）. Rabbits in Group N and D and the others were all fed with high fat forage. Neointima SMC apoptosis was detected by TUNEL method. SMC phenotypic modulation was studied with transmission electron microscope （TEM） and level of plasma angiotensin （Ang Ⅱ ） was measured with radioimmunity method. Results The plasma Ang Ⅱ level elevated gradually after feeding with high fat forage for 3 days, which led to denuded and injured abdominal artery. At 6 weeks, it showed significant difference compared with that in Group N （P〈0.01）. The plasma Ang Ⅱ level significanily reduced in Group G, as compared with that in Group C （P〈0.05）. Ang Ⅱ level in Group E and F showed the tendency to decrease. Apoptosis ceils appeared in Group A and more apoptosis cells appeared in Group B and C. Apoptosis cell positive expression rate in Group F and Group G was higher than that in Group C and it had an elevating tendency in Group E with no significant difference compared with that in Group C. Conclusion XSC could prevent AS onset and development by lowering plasma Ang Ⅱ level and promoting SMC apoptosis.