目的:研究灵仙新苷对动脉粥样硬化模型大鼠血脂的调节以及血管内皮细胞CD36、VCAM-1表达的影响。方法:SD大鼠随机分为空白对照组、模型对照组、辛伐他汀组(5 mg/kg)、灵仙新苷高剂量组(32 mg/kg)、灵仙新苷中剂量组(16 mg/kg)、灵仙新苷低剂量组(8 mg/kg)组。采用喂食高脂饲料及第1天一次性腹腔注射维生素D3复制大鼠动脉粥样硬化模型;造模第4周给予阳性药及受试药物,造模第12周大鼠眼眶取血,血清样本用于测定大鼠血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL),氧化型低密度脂蛋白(ox-LDL)水平。免疫组织化学法检测大鼠胸主动脉血管内皮细胞粘附分子-1(VCAM-1)和CD36的表达。结果:灵仙新苷能显著降低动脉粥样硬化大鼠血清TC、TG、LDL和ox-LDL水平,同时灵仙新苷能显著升高动脉粥样硬化大鼠血清HDL水平。免疫组织化学法结果显示灵仙新苷能够降低大鼠主动脉壁内皮细胞粘附分子(VCAM-1)和CD36的表达。结论:灵仙新苷能够有效调节动脉粥样硬化模型大鼠的血脂水平,减轻模型体内的氧化应激;灵仙新苷能够抑制VCAM-1介导的单核细胞与血管内皮细胞的粘附以及清道夫受体(CD36)介导巨噬细胞的内吞作用,灵仙新苷能有效抑制泡沫细胞的形成;灵仙新苷对动脉粥样硬化模型大鼠血脂的调节和抑制VCAM-1和CD36的表达对抑制动脉粥样硬化早期的动脉斑块形成有重要意义。 OBJECTIVE: To study the effects of LingXingGin on the regulation of blood lipids and the expressions of CD36 and VCAM-1 on vascular endothelial cells in atherosclerotic model rats. Methods: SD rats were randomly divided into blank control group, model control group, simvastatin group (5 mg / kg), Lingxinsin high dose group (32 mg / kg) mg / kg), Lingxinsin low dose group (8 mg / kg) group. The model of atherosclerosis was induced by feeding high-fat diet and the single intraperitoneal injection of vitamin D3 on the first day. The positive drug and the test drug were given in the fourth week of model making. To determine the level of total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein (HDL) and oxidized low density lipoprotein (oxLDL) in rats. Immunohistochemistry was used to detect the expression of vascular endothelial cell adhesion molecule-1 (VCAM-1) and CD36 in rat thoracic aorta. Results: Lingaxin can significantly reduce the levels of serum TC, TG, LDL and ox-LDL in atherosclerotic rats, and LingXingGan can significantly increase the level of serum HDL in atherosclerotic rats. Immunohistochemical results showed that Lingxianxin can reduce the expression of endothelial cell adhesion molecules (VCAM-1) and CD36 in the aortic wall of rats. CONCLUSION: Lingxianxin can effectively regulate the level of blood lipids in model rats with atherosclerosis and reduce the oxidative stress in vivo. Lingaxin can inhibit the adhesion of VCAM-1 to monocytes and vascular endothelial cells And scavenger receptor (CD36) mediated endocytosis of macrophages, Lingxindin can effectively inhibit the formation of foam cells; Lingxian glycosides in atherosclerosis model rats lipid regulation and inhibition of VCAM-1 And CD36 expression in the inhibition of atherosclerosis early plaque formation is of great significance.