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目的探讨替米沙坦在动脉粥样硬化(AS)形成过程中的作用及其机制。方法 40只SD大鼠随机分为四组,每组10只:AS组(A组)、替米沙坦4 mg.kg-1.d-18、mg.kg-1.d-1灌胃组(B1组、B2组)及正常对照组(C组)。采用套管法建立大鼠AS模型,并用替米沙坦干预。2周后,采用病理学方法观察动脉组织形态学变化,免疫组化法观察Rho相关卷曲螺旋形成蛋白激酶1(ROCK1)与单核细胞趋化蛋白1(MCP-1)的表达,Western blot检测ROCK1蛋白表达。结果 A组内膜增生,炎性细胞浸润,平滑肌细胞向内膜下迁移;而B1、B2组上述表现较A组明显减轻。B1、B2组ROCK1、MCP-1阳性细胞表达较A组减少。与C组相比,A组ROCK1蛋白表达增加(0.48±0.01 vs.2.13±0.02)(P<0.05);而B2组ROCK1蛋白表达较A组明显降低(0.94±0.01vs.2.13±0.02)(P<0.05)。结论替米沙坦通过减少Rho激酶与炎症因子MCP-1表达以达到抗AS的作用。
Objective To investigate the effect of telmisartan on the development of atherosclerosis (AS) and its mechanism. Methods Forty Sprague-Dawley rats were randomly divided into four groups (10 rats in each group): AS (group A), telmisartan 4 mg.kg-1.d-18, mg.kg-1.d-1 Group (group B1, group B2) and normal control group (group C). A rat model of AS was established by cannulation and intervention with telmisartan. Two weeks later, the morphological changes of arterial tissue were observed by pathological method. The expression of Rho-related curl-forming protein kinase 1 (ROCK1) and monocyte chemotactic protein 1 (MCP-1) were observed by immunohistochemistry. ROCK1 protein expression. Results A group of intimal hyperplasia, inflammatory cell infiltration, smooth muscle cells to submucous migration; and B1, B2 group than the A group was significantly reduced. The expression of ROCK1 and MCP-1 positive cells in B1 and B2 groups decreased compared with that in A group. Compared with group C, the expression of ROCK1 protein in group A increased (0.48 ± 0.01 vs.2.13 ± 0.02) (P <0.05), while the expression of ROCK1 in group B2 was significantly lower than that in group A (0.94 ± 0.01 vs.2.13 ± 0.02) P <0.05). Conclusion Telmisartan can inhibit the expression of Rho kinase and inflammatory cytokines MCP-1.