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