固本化痰通脉方对痰阻血脉大鼠主动脉巨噬细胞和黏附分子表达的影响

Effects of Guben Hutan Tongmai Recipe on expressions of macrophages and cell adhesion molecules of aortic endothelia in rats with syndrome of phlegm blocking blood vessel

目的:观察固本化痰通脉方对痰阻血脉大鼠主动脉巨噬细胞和黏附分子表达的影响,探讨痰邪的致病机制。方法:7周龄正常雄性Wistar大鼠50只随机分为正常对照组、模型组、固本化痰通脉方低剂量组、固本化痰通脉方高剂量组、辛伐他汀对照组5组,在高脂饮食基础上建立痰证模型,比较各组大鼠血脂代谢的改变,免疫组化方法观察主动脉内皮巨噬细胞和细胞间黏附分子-1(intercellularadhesionmolecule-1,ICAM-1)、血管细胞黏附分子-1(vascularcelladhesionmolecule-1,VCAM-1)、P-选择素、E-选择素的表达,并经图像分析定量。结果:与正常对照组相比,模型组血脂水平、巨噬细胞和黏附分子的表达差异有统计学意义(P<0.01);各治疗组与模型组相比差异有统计学意义(P<0.05)。结论:固本化痰通脉方能降低血清胆固醇、甘油三酯,升高高密度脂蛋白水平,抑制主动脉内皮巨噬细胞、ICAM-1、VCAM-1、P-选择素和E-选择素的表达。

Objective： To observe the effects of Guben Huatan Tongmai Recipe （GBHTTMR）, a compound Chinese herbal recipe, on expressions of macrophages and cell adhesion molecules （CAMs） of aortic endothelia in rats with syndrome of phlegm blocking blood vessel, and to explore the pathogenesis of the phlegm-pathogen. Methods： Fifty normal male Wistar rats, 7-week in age, were randomly divided into five groups： normal control group, untreated group, high-dose GBHTTMR-treated group, low-dose GBHTTMR-treated group and simvastatin-treated group, with 10 rats in each group. Syndrome of phlegm blocking blood vessel was induced in rats of the latter 4 groups by feeding the rats with high lipid diet. Levels of blood lipid were compared among the 5 groups. The expressions of macrophages and CAMs in aortic endothelia were tested by immunohistochemical staining method. Results： The level of blood lipid, and the expressions of macrophages and CAMs showed statistical differences between the normal control group and the untreated group （P 〈 0.01）, and between the untreated group and the low-, high-dose GBHTTMR-treated and simvastatin-treated groups as well （P 〈 0.05）. Conclusions： GBHTTMR can decrease the level of serum cholesterol and triglycerides, and increase the level of high density lipoprotein. It also can inhibit the expressions of macrophages, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, P-selectin, and E-selectin.