二苯乙烯苷对动脉粥样硬化大鼠主动脉胞间粘附分子1、血管细胞粘附分子1及血管内皮生长因子表达的影响

目的探讨二苯乙烯苷(TSG)抗动脉粥样硬化(AS)的可能机制。方法采用高脂饲料喂饲+维生素D37MU·kg-1ip1次制备大鼠AS模型。造模12周后治疗性ig给予TSG30,60和120mg·kg-1·d-1。给药6周后,采用黄嘌呤氧化酶法测定血清超氧化物歧化酶(SOD)活性,硫代巴比妥酸比色法测定血清丙二醛(MDA)含量,Western蛋白印迹法检测主动脉胞间粘附分子1(ICAM-1)、血管细胞粘附分子1(VCAM-1)及血管内皮生长因子(VEGF)的表达,逆转录聚合酶链反应法检测主动脉ICAM-1和VCAM-1 mRNA表达,免疫组织化学法检测主动脉VEGF蛋白的表达。结果与正常组相比,AS模型组大鼠血清SOD活性明显降低,MDA水平明显提高,主动脉ICAM-1,VCAM-1及VEGF mRNA和蛋白表达显著增高。与模型组相比,TSG给药6周能明显提高大鼠血清SOD活性,降低MDA水平,对主动脉ICAM-1,VCAM-1及VEGF mRNA和蛋白表达均有明显抑制作用。结论TSG对大鼠实验性AS具有治疗作用,其机制可能与其抗氧化和调节细胞因子分泌有关。

Effects of 2, 3, 4′, 5-tetrahydroxystilbene-2-O-β-D glucoside on expressions of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and vascular endothelial growth factor in aorta of atherosclerotic rats

AIM To study the mechanisms of 2, 3, 4′, 5-tetrahydroxystilbene-2-O-β-D glucoside(TSG) for its antiatherosclerotic effect. METHODS Male SD rats were fed with high fat diet for 12 weeks and ip vitamin D₃ 7 MU·kg^-1, 1 time, to establish atherosclerosis (AS) model. The AS rats were treated with TSG 30, 60 and 120 mg·kg^-1·d^-1, ig, respectively, for 6 weeks. Western blot was used to determine the expression of aorta intercellular adhesion molecul-1 (ICAM-1), vascular cell adhesion molecule-1(VCAM-1) and vascular endothelial growth factor (VEGF) protein. RT-PCR was used in detection of the expression of ICAM-1 and VCAM-1 mRNA, and immunohistochemical method was used to detect the changes of VEGF protein expression. The malonaldehyde (MDA) level and superoxide dismutase (SOD) activity in serum were also determined. RESULTS Compared with the normal control, the SOD activity decreased and MDA level increased markedly in serum, and the expressions of ICAM-1, VCAM-1 and VEGF in atherosclerotic aorta increased remarkably in model group. However, compared with the model, the serum SOD activity increased and the level of MDA decreased markedly, and the expressions of ICAM-1, VCAM-1 and VEGF in atherosclerotic aorta decreased remarkably after administering TSG. CONCLUSION TSG shows antiatherosclerotic effect by anti-oxydation and modulation of the adhesion molecule expression.