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

摘要

Ojective To investigate the effects of fasudil hydrochloride on injury of HUVECs induced by Ang Ⅱ which influences the expression of Rho-associated kinase(ROCK) and monocyte chemoattractant protein-1(MCP-1).Methods HUVECs which were incubated in vitro were divided into control group, Ang Ⅱ 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 Ⅱ significantly decreased the production of NO in endothelial cells (P ＜ 0.01).Compared with Ang Ⅱ group,in the specific blocker 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 kinase signaling pathways,thus inhibiting occurrence and development of atherosclerosis.%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)Rho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、Ang Ⅱ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Ang Ⅱ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Ang Ⅱ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Ang Ⅱ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.