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目的:观察奥美沙坦对兔血管内膜损伤后过氧化物酶体增殖物激活受体γ(PPARγ)及单核细胞趋化蛋白1(MCP-1)表达的影响,探讨奥美沙坦预防动脉粥样硬化的可能机制。方法:雄性新西兰大白兔24只,随机分为3组:普通饲料喂养组(G1),高脂饮食喂饲加动脉内皮损伤组(G2),高脂饮食喂饲加动脉内皮损伤组加奥美沙坦治疗组(G3)。G2、G3组持续给予1.5%的胆固醇喂养2周后行腹主动脉内膜剥脱术,G3组内膜剥脱术后第1天开始口服奥美沙坦10mg.kg-1.d-1。3组均于8周后取兔腹主动脉行病理形态学观察,RT-PCR方法检测各组PPARγ和MCP-1mRNA的表达。结果:高胆固醇喂养8周后,G3组较G2组内膜厚度减少71%,内膜面积减少37%,内膜厚度与中膜厚度比减少34%,内膜面积与中膜面积比减少31%。G2组较G1组,PPARγ和MCP-1均表达增加,G3组PPARγ表达高于G2组(P<0.05),而MCP-1表达低于G2组(P<0.05)。结论:奥美沙坦可明显抑制血管损伤后的内膜增生并改善血管重构,其机制可能与调节PPARγ,从而影响MCP-1水平,改善动脉粥样硬化有关。
OBJECTIVE: To observe the effect of olmesartan on the expression of peroxisome proliferator-activated receptor γ (PPARγ) and monocyte chemotactic protein-1 (MCP-1) after vascular intimal injury in rabbits and to explore the protective effect of olmesartan on the prevention of arterial Possible mechanisms of atherosclerosis. Methods: Twenty-four male New Zealand white rabbits were randomly divided into three groups: normal diet group (G1), high fat diet group fed with arterial endothelial injury group (G2), high fat diet fed with arterial endothelial injury group Tan treatment group (G3). G2, G3 group continued to give 1.5% cholesterol for 2 weeks after abdominal aortic endarterectomy, G3 endarterectomy after the first day of oral administration of olmesartan 10mg.kg-1.d-1.3 group were The pathological morphological changes of rabbit abdominal aorta were observed after 8 weeks. The expression of PPARγ and MCP-1 mRNA in each group were detected by RT-PCR. RESULTS: After hypercholesterolemia for 8 weeks, the thickness of intima in G3 group decreased 71%, the intima area decreased 37%, the intima thickness and intima-media thickness decreased 34%, the intima-media area ratio decreased 31 %. The expression of PPARγ in G3 group was higher than that in G2 group (P <0.05), while the expression of MCP-1 was lower in G2 group than in G2 group (P <0.05). Conclusion: Olmesartan can significantly inhibit neointimal hyperplasia and vascular remodeling after vascular injury, and its mechanism may be related to the regulation of PPARγ, thereby affecting the level of MCP-1 and improving atherosclerosis.