盐酸法舒地尔对血管紧张素Ⅱ诱导内皮细胞的炎性保护作用  

Protective effect of fasudil hydrochloride against inflammation of endothelial cells induced by angiotensinⅡ in vitro

作　　者：杨雪佳[1] 王高频[1] 王继红[2] 刘国銮[1] 马海芳[1] 

机构地区：[1]辽宁医学院附属第一医院心内科二病区,锦州121001 [2]辽宁中医药大学

出　　处：《中华老年心脑血管病杂志》2011年第5期449-451,共3页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

摘　　要：目的探讨盐酸法舒地尔对血管紧张素Ⅱ(AngⅡ)诱导的人脐静脉血管内皮细胞(HUVECs)Rh0激酶和单核细胞趋化蛋白1(MCP-1)表达的影响。方法将体外培养的HUVECs分为对照组、AngⅡ组、阻断剂组和药物组。硝酸还原酶法测NO含量,免疫细胞化学法测MCP-1蛋白定位表达,蛋白印迹法测Rho激酶和MCP-1蛋白定量表达。结果与对照组比较,其他3组NO含量显著减少(P<0.01);阻断剂组、药物组NO含量较AngⅡ组显著升高(P<0.01);药物组与阻断剂组无显著差异(P>0.05)。与AngⅡ组比较,阻断剂组和药物组Rho激酶及MCP-1蛋白表达显著降低(P<0.01),但高于对照组(P<0.01);2组蛋白表达无显著差异(P>0.05)。结论盐酸法舒地尔可对AngⅡ诱导的HUVECs产生保护作用,通过降低内皮细胞的炎性反应起保护作用。Ojective To investigate the effects of fasudil hydrochloride on injury of HUVECs induced by Ang 11 which influences the expression of Rho-associated kinase（ROCK） and monocyte chemoattractant protein-l（MCP-1）. Methods HUVECs which were incubated in vitro were divided into control group, Ang 11 group, specific blocker group and drug group. MCP-1 was observed using immunocytochemistry. Quantitative expression of ROCK and MCP 1 was measured by Western blot. Results Compared with control group, Ang 1I significantly decreased the production of NO in endothelial cells （P 〈 0.01）. Compared with Ang Ⅱ group,in the specific bloc ker group and the drug group, the production of NO was significantly increased and the expression of ROCK and MCP-1 was significantly decreased,but they were still higher than those in the control group （P 〈 0.01）. Conclusion Fasudil hydrochloride can protect against injury of HUVECs induced by Ang Ⅱ , through controlling the expression of ROCK and MCP-1 in the Rho/Rho ki- nase signaling pathways,thus inhibiting occurrence and development of atherosclerosis.

关 键 词：动脉粥样硬化 RHO相关激酶类 血管紧张素Ⅱ 内皮细胞 趋化因子CCL2 一氧化氮 脐静脉 

分 类 号：R965[医药卫生—药理学]