中文摘要：

目的观察高糖和高胰岛素对几个调控血管平滑肌细胞（VSMC）舒缩功能信号分子的作用，探讨糖尿病并发高血压的分子机制。方法将培养的大鼠主动脉VSMC随机分成对照组、高糖组（葡萄糖浓度25mmol／L）、高胰岛素组（胰岛素浓度50 μU／ml）、高糖＋高胰岛素组、生理浓度胰岛素组（胰岛素浓度10μU／ml）、高糖＋生理浓度胰岛素组。蛋白免疫印迹法测定细胞诱导型一氧化氮合酶（iNOS）、内皮型一氧化氮合酶（eNOS）、小分子鸟苷酸蛋白A（RhoA）、Rho激酶-1（ROCK-1）蛋白表达，比率荧光倒置显微镜检测细胞内钙水平（[Ca^2＋]i）。结果高糖组iNOS、eNos表达减少，[Ca^2＋]i升高，RhoA、ROCK-1表达明显升高；高胰岛素组iNOS、eNos表达明显升高，[Ca^2＋]i明显降低，RhoA、ROCK-1无明显改变；生理胰岛素组iNOS、eNOS表达明显升高，[Ca^2＋]i、RhoA、ROCK-1无明显改变；当同时给予胰岛素和葡萄糖刺激时，胰岛素可拮抗高糖对上述4种分子的蛋白表达及[Ca^2＋]i的增加。结论高糖损害VSMC正常收缩舒张功能，而胰岛素可拮抗高糖对VSMC收缩舒张功能的损害作用。

英文摘要：

Objectlve To investigate the influence of high glucose or/and insulin on expression of several signaling molecules of vascular smooth muscle cells and the molecular mechanism of diabetes mellitus complicated by hypertension. Methods Cultured vascular smooth muscle cells from rat were randomly divided into the following groups： control, high glucose （HG）, high insulin （HI）, high glucose and high insulin （ HG ＋ HI ）, high glucose and normal insulin（HG ＋ NI） and normal insulin（NI）. Western blot was used to detect the expression of iNOS,eNOS,RhoA,ROCK-1 of each group. The fluorescence microscope was used for the detection of intracellular Ca^2＋ level. Results The expression of iNOS or eNOS in HG group was decreased, in contrast, the intracellular Ca^2＋ level and the expression of RhoA or ROCK-1 were increased. In HI group,the expression of iNOS or eNOS was increased, while the intracellular Ca^2＋ level was reduced and the expression of RhoA or ROCK- 1 had no change. In NI group, iNOS or eNOS expression was increased, while the others were same as those in control group. In HG ＋ HI group or HG ＋ NI group, insulin had the effect against the impact of glucose on vascular smooth muscle cells. Conclusion High glucose has an injurious effect on relaxation and contraction of VSMC, while insulin can conteract this effect.