中文摘要：

目的 观察苦丁茶对动脉粥样硬化大鼠血管内皮功能的影响.方法 将60只SD大鼠随机分为对照组、模型组、血脂康组（0.11 g/kg）、苦丁茶高剂量组（4.64 g/kg）、苦丁茶中剂量组（2.32 g/kg）、苦丁茶低剂量组（1.16 g/kg）.除对照组用常规饲料喂养外,其余5组均以高脂饲料加一次性注射维生素D建立实验性动脉粥样硬化大鼠模型,治疗组在造模同时给予不同剂量的药物干预.8周后,测定各组血脂、观察动脉内膜形态学改变及主动脉壁细胞间黏附分子-1（ICAM-1）的表达水平.结果 苦丁茶各组血清TG、TC、LDL-C有不同程度的降低,HDL-C升高,其中苦丁茶高剂量组最明显（P＜0.05）；形态学显示苦丁茶各组主动脉内皮损伤程度较模型组减轻；免疫组化结果显示,模型组大鼠主动脉内皮细胞ICAM-1表达强阳性,苦丁茶高剂量组动脉血管壁ICAM-1的表达水平显著下调（P＜0.05）；苦丁茶高剂量组与血脂康组效果相当（P＞0.05）.结论 苦丁茶能有效调节动脉粥样硬化大鼠血脂的异常、降低ICAM-1表达,减轻内皮细胞损伤,其中以高剂量组作用最显著,这可能是其抗动脉粥样硬化的作用机制之一.

英文摘要：

Objective： To observe the effect of Ilex kudingcha on epithelial function of atherosclerosis model rats. Method： Sixty healthy SD rats were randomly divided into Control group ,Model group ,Xuezhikang group（0.11 g/ kg） ,High dose Ilex kudingcha decoction group（4.64 g/kg）,Middle dose Ilex kudingcha decoction group （2.32 g/ kg）and Low Ilex kudingcha decoction group （1.16 g/kg）. In addition to control group which was fed with normal diet,other five groups were fed with high-fat diet plus Vitamin D injection to establish the experimental AS rat model. While modeling,the treatment groups were given different drug doses of intervention. After 8 weeks,the level of blood lipid,the morphological characteristics of the aorta and the expression of ICAM-1 level in aorta of each group were observed. Result： Ilex kudingcha of each group could lower serum TC,TG,LDL-c and increase HDL-c. By comparing High dose Ilex kudingcha decoction group with model group ,the difference had statistical significance （P〈 0.05）. The morphological results of Ilex kudingcha groups reveal that aortic endothelial injury was slighter than that of model group. The results of immunohistochemistry showed a strong positive ICAM-1 expres- sion level in model group. High dose Ilex kudingcha decoction group could significantly reduce the expression level of ICAM-1 of the arterial wall （P〈 0.05 ）. There was no significant difference between High dose Ilex kud- ingcha and Xuezhikang group. Conclusion： Ilex kudingcha can effectively regulate blood lipid of AS rats, reduce ICAM-1 expression and alleviate the injury of endothelial cells. The effect of high dose group is the most obvi- ous, which may be one of the mechanisms of anti-AS.