上海交通大学学报（医学版）

›› 2013, Vol. 33 ›› Issue (1): 19-.doi: 10.3969/j.issn.1674-8115.2013.01.004

• 论著（基础研究） • 上一篇    下一篇

瑞舒伐他汀对高糖导致的血管形成障碍的影响

王法斌, 李京波, 朱 伟, 李 帅, 余 涛, 魏 盟   

  1. 上海交通大学附属第六人民医院心内科, 上海 200233
  • 出版日期:2013-01-28 发布日期:2013-02-06
  • 通讯作者: 李京波, 电子信箱: jbli@medmail.com.cn。
  • 作者简介:王法斌（1983—）, 男, 硕士生；电子信箱: wangfabin_2006@yahoo.cn。

Effect of rosuvastatin on impaired angiogenesis induced by hyperglycemia

WANG Fa-bin, LI Jing-bo, ZHU Wei, LI Shuai, YU Tao, WEI Meng   

  1. Department of Cardiology, the Sixth People´s Hospital, Shanghai Jiaotong University, Shanghai 200233, China
  • Online:2013-01-28 Published:2013-02-06

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摘要：

目的 探讨瑞舒伐他汀对高糖导致的血管形成障碍的影响。方法 培养原代心肌微血管内皮细胞，取1代细胞分为四组：低糖组（5.6 mmol/L葡萄糖）、高糖组（33.3 mmol/L葡萄糖）、瑞舒伐他汀组（33.3 mmol/L葡萄糖+1 μmol/L瑞舒伐他汀）和LY294002组（33.3 mmol/L葡萄糖+1 μmol/L瑞舒伐他汀+10 μmol/L LY294002），其中LY294002为磷脂酰肌醇3-激酶（PI3K）的抑制剂。采用Matrigel、Transwell和MTT法分别观察四组微血管内皮细胞的管腔形成、迁移及增殖能力。采用Western blotting技术检测蛋白激酶B（Akt）、磷酸化Akt（Ser473）（p-Akt）、内皮一氧化氮合酶（eNOS）和磷酸化eNOS（Ser1117）（p-eNOS）蛋白的表达。结果 与低糖组相比，高糖组的内皮细胞管腔形成、迁移及增殖能力均明显降低（P<0.05）；瑞舒伐他汀组的内皮细胞管腔形成、迁移及增殖能力均明显高于高糖组及LY294002组，但仍低于低糖组，差异均有统计学意义（P<0.05）。瑞舒伐他汀组p-Akt和p-eNOS蛋白的相对表达量均明显高于高糖组和LY294002组（P<0.05），并基本恢复至低糖组水平（P>0.05）。结论 瑞舒伐他汀可明显改善高糖导致的内皮细胞的血管形成障碍，其机制可能与激活PI3K/Akt/eNOS通路相关。

关键词: 瑞舒伐他汀, 高糖, 血管生成

Abstract:

Objective To investigate the effect of rosuvastatin on impaired angiogenesis induced by hyperglycemia. Methods Primary microvascular endothelial cells of myocardium were cultured. Cells of passage one were randomly divided into low-glucose group (5.6 mmol/L glucose), high-glucose group (33.3 mmol/L glucose), rosuvastatin group (33.3 mmol/L glucose+1 μmol/L rosuvastatin) and LY294002 (phosphatidylinositol 3-kinase inhibitor) group (33.3 mmol/L glucose +1 μmol/L rosuvastatin+10 μmol/L LY294002). Matrigel, Transwell and MTT assays were used to evaluate the ability of tube formation, migration and proliferation of endothelial cells respectively. Moreover, Western blotting was employed to detect the protein expression of protein kinase B (Akt), phosphoAkt (Ser473)(p-Akt), endothelial nitric oxide synthase (eNOS) and phospho-eNOS(Ser1117)(p-eNOS). Results The ability of tube formation, migration and proliferation of endothelial cells in highglucose group was significantly lower than that in low-glucose group (P<0.05). The ability of tube formation, migration and proliferation of endothelial cells in rosuvastatin group was significantly higher than that in high-glucose group and LY294002 group (P<0.05), but was significantly lower than that in low-glucose group (P<0.05). The relative expression of p-Akt and p-eNOS protein in rosuvastatin group was significantly higher than that in high-glucose group and LY294002 group (P<0.05), but was not significantly different from that in low-glucose group (P>0.05). Conclusion Rosuvastatin can significantly improve hyperglycemia-induced impaired angiogenesis in endothelial cells, the mechanism of which may be associated with the activation of PI3K/ Akt/eNOS pathway.

Key words: rosuvastatin, hyperglycemia, angiogenesis