黄连温胆汤对MS模型大鼠血管细胞黏附分子-1和细胞间黏附分子-1表达的影响

Influence of Huanglian Wendan Decoction on Vascular Cell Adhesion Molecule-1 and Intercellular Adhesion Molecule-1 of MS rats

目的:研究黄连温胆汤对MS模型大鼠血管损害相关因素的影响。方法:建立MS模型,高脂高盐高糖饲料喂养雄性SD大鼠20周,37只成模,将其随机分为模型组、黄连温胆汤高、低剂量组、二甲双胍组,各个组间分别灌服相对应药物。4周后,免疫组化法检测大鼠主动脉核因子-κB的表达,逆转录聚合酶链式反应检测血管细胞黏附分子-1和细胞间黏附分子-1相对定量表达情况。结果:加减黄连温胆汤高剂量组和二甲双胍组大鼠核因子-κB表达均显著降低(P<0.01),二组间比较无显著性差异(P>0.05),加减黄连温胆汤低剂量组核因子-κB表达显著降低(P<0.01)。在血管细胞黏附分子-1和细胞间黏附分子-1表达相对量方面,加减黄连温胆汤高剂量组和MF组均较模型组显著降低(P<0.01),并且组间比较无显著性差异(P<0.01)。结论:加减黄连温胆汤能抑制核因子-κB激活,进一步抑制血管细胞黏附分子-1和细胞间黏附分子-1表达,保护血管内皮细胞,防治早期靶器官血管内皮功能紊乱。

Objective：To study the mechanism of Huanglian Wendan Decoction in preventing and treating MS. Method：We established MS model by high fat and high salt diet in male SD rats for 20 weeks. 37 were successful,which were randomly divided into model group,Huanglian Wendan Decoction high and low dose groups,metformin group. Each group was given the corresponding drugs for 4 weeks. After drug intervention,immunohistochemistry was used to detect the expression of nuclear factorkappa B in rat aorta,reverse transcriptase polymerase chain reaction for the detection of vascular cell adhesion molecule1 and intercellular adhesion molecule- 1relative quantitative expression. Result：The nuclear factor kappa B expression in model group was increased significantly（P〈0.01）. After intervention for 4 weeks,modified Huanglian Wendan Decoction high dose group and metformin group＇s nuclear factor kappa B expressions were significantly lower（P〈0.01）and the two groups had no significant difference（P〈0.05）. The modified Huanglian Wendan Decoction low dose group＇s nuclear factor kappa B expression was significantly lower（P〈0.01）. The vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expressions of modified Huanglian Wendan Decoction high dose group and MF group were significantly lower than those in the model group（P〈0.01）and the comparison group showed no significant difference（P〈0.01）. Conclusion：Modified Huanglian Wendan Decoction can inhibit aorta nuclear factor kappa B activation and further inhibit the expressions of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 to protect the vascular endothelial cells and prevent endothelial dysfunction of early target organs.