虎杖苷对动脉粥样硬化大鼠血脂的调节和CD36、VCAM-1表达的影响

Effects of Polydatin on the Regulation of Blood Lipid and Expressions of CD36,VCAM-1 in Atherosclerotic Rats

目的探讨虎杖苷对动脉粥样硬化(AS)大鼠血脂的调节以及血管内皮细胞清道夫受体(CD36)、细胞黏附分子-1(VCAM-1)表达的影响。方法 SD大鼠随机分为6组:正常对照组、模型组、辛伐他汀组(5mg·kg^(-1))、虎杖苷高、中、低剂量(160mg·kg^(-1)、80mg·kg^(-1)、40mg·kg^(-1))组。以高脂饲料喂养及腹腔注射维生素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,分别于造模前、造模后第4周、8周、12周记录体重;第12周大鼠眼眶取血,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)水平;取肝脏进行常规HE染色,观察肝脏病变;免疫组织化学法检测大鼠胸主动脉血管内皮VCAM-1和CD36的表达。结果虎杖苷能显著降低动脉粥样硬化大鼠血清TC、TG、LDL水平,显著升高动脉粥样硬化大鼠血清HDL水平;改善肝脏的脂肪变性和炎症细胞浸润;降低大鼠主动脉壁内皮细胞VCAM-1和CD36的表达。结论虎杖苷能够有效调节动脉粥样硬化模型大鼠的血脂水平,抑制CD36介导的巨噬细胞内吞作用和VCAM-1介导的单核细胞与血管内皮细胞黏附,有效抑制泡沫细胞的形成。

Objective To investigate the effect of polydatin on blood lipid and the expression of scavenger receptor CD36 and cell adhesion molecule-1（ VCAM-1） in atherosclerotic rats. Methods Sprague-Dawley rats were divided randomly into six groups： native group,model group,simvastatin group（ 5 mg·kg^（-1））,high dosage of polydatin group（ 160 mg·kg^（-1））,middle dosage of polydatin group（ 80 mg·kg^（-1）） and low dosage of polydatin group（ 40 mg · kg^（-1））. Model was established by feeding with high fat diet and injecting vitamin D3 intraperitoneally,positive drugs and tested drugs were given in the 4 th week to the model,body weight was recorded in the 4 th,8 th and 12 th week after the establishment of the model. Serum triglyceride（ TG）,total cholesterol（ TC）,high density lipoprotein（ HDL）,low density lipoprotein（ LDL） were measured in the 12 th week. The liver lesions were observed by HE staining. Immunohistochemical method was used to detect the expression of VCAM-1 and CD36 in rat thoracic aorta endothelium. Results Polydatin can significantly decrease the level of serum TG,TC,LDL; increase the serum level of HDL; improve hepatic steatosis and inflammatory cell infiltration; decrease the expression of VCAM-1 and CD36 in atherosclerotic rats. Conclusion Polydatin can effectively regulate the lipid level of atherosclerotic rats,inhibit the adhesion of monocytes mediated by VCAM-1 to vascular endothelial cells and the endocytosis of macrophages mediated by CD36,and inhibit the formation of foam cells.