RESUMEN
Aim To investigate the effect of simvastatin ( Sim ) on endogenous antioxidant system after acute myocardial infarction ( AMI ) and its potential mecha-nisms. Methods The acute myocardial infarction ( AMI ) rat models were made by ligation left anterior descending of coronary artery. Then the successful models were randomly divided into myocardial infarc-tion group ( MI group) and simvastatin group ( Sim,20 mg·kg-1·d-1), another group without ligation left anterior descending of coronary artery served as sham group(Sham group). The Sim group was administered simvastatin by gavage for 7 days. MI group and Sham group received saline. Hemodynamic parameters, lipid levels, troponinI ( c-TnI ) and lactate dehydrogenase ( LDH) concentrations were examined after 7days, and the levels of superoxide dismutase ( SOD) and glutathi-one peroxidase ( GP) of myocardial antioxidant system were detected by ELISA. The expression of cardiac p-Akt and p-eNOS protein were detected by Western blot. Results Acute myocardial infarction significant-ly lowered cardiac hemodynamic parameters, increased serum c-TnI and LDH levels, lowered levels of SOD and GP, and lowered the expression of p-Akt and p-eNOS protein. However, Sim could effectively prevent the deterioration of cardiac function, reduce serum c-TnI and LDH levels, increase levels of SOD and GP, and increase p-Akt and p-eNOS protein expression. Conclusion Early using Sim can effectively improve heart function after acute myocardial infarction, acti-vate myocardial antioxidant system,and reduce myocar-dial necrosis, which may be related to increasing the expression of p-Akt and p-eNOS.
RESUMEN
Objective: To explore the effect of resveratrol (Res) on angiogenesis of human umbilical vein endothelial cells (HUVEC) with the possible mechanisms in vitro. Methods: The HUVECs were cultured in 6 groups.①Control group, HUVEC were cultured with high glucose in DMEM,②Res group, the cell were cultured with Res at different concentrations,③Res with PI3K blocker LY294002 (Res+Blocker 1) group, ④Blocker 1 group, HUVEC were cultured with LY294002 alone, ⑤Res with eNOS blocker L-NAME (Res +Blocker 2) group and ⑥Blocker 2 group. The effect of Res on HUVEC proliferation was detected by CCK-8 kit, the protein expressions of p-Akt, p-eNOS were examined by Westin blot analysis, nitric oxide (NO) level was measured by nitrate reduction method and the endothelial cell migration was assayed by transwell chamber method. Results: ① Compared with Control group, HUVEC proliferation increased in Res (1, 5μmol/L ) group, P0.05.④Compared with Control group, the cell migration and tubing formation were higher in Res (5μmol/L) group, P Conclusion: Res could up-regulate NO level via activating PI3-K/Akt/eNOS signaling and therefore, improving the proliferation, migration and tubing formation of HUVEC in vitro.