Effect of demethylasterriquinone b1 in hypertension associated vascular endothelial dysfunction.
Effect of demethylasterriquinone b1 in hypertension associated vascular endothelial dysfunction.
复制标题
去甲基星三醌 b1 对高血压相关血管内皮功能障碍的影响。
DOI：
10.1016/j.ijcard.2006.10.006
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发表时间：
2007
影响因子：
3.5
通讯作者：
Singh,Manjeet
中科院分区：
文献类型：
--
作者：
Shah,DhvanitI;Singh,Manjeet
背景Akt 的激活刺激 eNOS 的磷酸化、一氧化氮的产生并减少氧化应激。该研究旨在研究 DAQ B1（一种 Akt 激活剂）在高血压相关血管内皮功能障碍中的作用。方法将大鼠进行肾切除，并给予大鼠 DOCA（40 mg kg−1，皮下注射）以产生高血压（MABP>140 mm Hg）。使用分离的主动脉环制备物、胸主动脉电子显微镜和亚硝酸盐/硝酸盐的血清浓度来评估血管内皮功能障碍。通过逆转录聚合酶链反应评估 p22phox 和 eNOS 信使 RNA 的表达。评估血清 TBARS 和主动脉超氧阴离子以评估氧化应激。 结果 DAQ B1（5 mg kg−1，口服）或阿托伐他汀（30 mg kg−1，口服）显着改善高血压患者的乙酰胆碱诱导的内皮依赖性舒张、血管内皮衬里、eNOS 和 p22phox mRNA 的表达、血清亚硝酸盐/硝酸盐浓度和血清 TBARS老鼠。然而，DAQ B1 的这种改善作用已被 eNOS 抑制剂 l-NAME（25 mg kg−1，腹腔注射）所阻止。结论因此，可以得出结论，DAQ B1 诱导的 Akt 激活可能会激活 eNOS，从而减少氧化应激，从而改善高血压相关的血管内皮功能障碍。
BACKGROUNDActivation of Akt stimulates phosphorylation of eNOS, production of nitric oxide and reduces oxidative stress. The study has been designed to investigate the effect of DAQ B1, an activator of Akt, in hypertension associated vascular endothelial dysfunction.METHODSRats were uninephroctomized and DOCA (40 mg kg−1, s.c.) was administered to rats to produce hypertension (MABP>140 mm Hg). Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, electron microscopy of thoracic aorta and serum concentration of nitrite/nitrate. The expression of messenger RNA for p22phox and eNOS was assessed by reverse transcription-polymerase chain reaction. Serum TBARS and aortic superoxide anion were estimated to assess oxidative stress.RESULTSDAQ B1 (5 mg kg−1, p.o.) or atorvastatin (30 mg kg−1, p.o.) markedly improved acetylcholine induced endothelium dependent relaxation, vascular endothelial lining, expression of mRNA for eNOS and p22phox, serum nitrite/nitrate concentration and serum TBARS in hypertensive rats. However, this ameliorative effect of DAQ B1 has been prevented by l-NAME (25 mg kg−1, i.p.), an inhibitor of eNOS.CONCLUSIONTherefore, it may be concluded that DAQ B1 induced activation of Akt may activate eNOS and consequently reduce oxidative stress to improve hypertension associated vascular endothelial dysfunction.