目的 探讨阿托伐他汀对血管紧张素Ⅱ( AngⅡ)诱导的人脐静脉内皮细胞(HUVEC) Rho/Rho激酶信号通路中Rho激酶和磷酸化肌球蛋白轻链(p-MLC)表达的影响.方法 体外培养HUVEC,分4组:对照组；AngⅡ组；阻断剂组(Rho激酶阻断剂Y-27632);阿托代他汀组.硝酸还原酶法检测NO含量;免疫细胞化学法观察p-MLC蛋白定位表达,Western blot法测定Rho激酶和p-MLC蛋白定量表达.结果 与对照组比较,AngⅡ组NO含量显著减少(P＜0.01)；阻断剂组和阿托伐他汀组NO含量较AngⅡ组显著升高(P＜0.01).AngⅡ组细胞质内出现大量棕色颗粒积聚、浓染；阻断剂组和阿托伐他汀组细胞质中仅有少量棕色淡染颗.与AngⅡ组比较,阻断剂组和阿托伐他汀组Rho激酶及p-MLC蛋白表达显著降低(P＜0.01),但仍高于对照组(P＜0.01);2组间蛋白表达仍有明显差异(P＜0.01).结论 阿托伐他汀对AngⅡ诱导的HUVEC保护作用,是通过抑制Rho/Rho激酶信号通路中Rho激酶及其下游的p-MLC蛋白表达,减弱AngⅡ对内皮细胞骨架的损伤.%Ojective To study the effect of atorvastatin on expression of Rho kinase and phospho-rylated myosin light chain (p-MLC) in angiotensin II (Ang H Hnduced Rho/Rho kinase signal pathway of human umbilical vein endothelial cells (HUVEC). Methods HUVEC, cultured in vitro, were divided into normal control group, Ang H group, Rho kinase blocker Y-27632 group, and atorvastatin group. Nitric oxide (NO) level in HUVEC was measured by nitrate reduction test. Expression of p-MLC protein and Rho kinase in HUVEC was detected by immunocytochem-istry and Western blot, respectively. Results The NO level was significantly lower in Ang II group than in control group and significantly higher in Rho kinase blocker Y-27632 group than in atorvastatin group(P<0. 01). A large number of brown and hyperchromatic granules were accumulated in cytoplasm of Ang fl group while a small number of brown and hypochromatic granules were accumulated in cytoplasm of Rho kinase blocker Y-27632 group and atorvastatin group. Although the expression level of Rho kinase and p-MLC protein decreased significantly in Rho kinase blocker Y-27632 group and Ang FJ group, it was still higher than that in control group(P< 0. 01). Conclusion Atorvastatin can protect Ang E-induced HUVEC by controlling the expression of Rho kinase and its downstream p-MLC protein in Rho/Rho kinase signaling pathway and weakening the Ang H -induced endothelial cytoskeleton injury.
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