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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Possible role of Akt to improve vascular endothelial dysfunction in diabetic and hyperhomocysteinemic rats.
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Possible role of Akt to improve vascular endothelial dysfunction in diabetic and hyperhomocysteinemic rats.

机译：在糖尿病和高同型半胱氨酸血症大鼠中，Akt可能改善血管内皮功能障碍。

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The study has been designed to investigate the effect of demethylasterroquinone B1 (DAQ B1), an activator of Akt, in diabetes mellitus (DM) and hyperhomocysteinemia (HHcy)-induced vascular endothelial dysfunction. Streptozotocin (55 mg kg(-1), i.v.) and methionine (1.7% w/w, p.o., 4 weeks) were administered to rats to produce DM (serum glucose >140 mg dl(-1)) and HHcy (serum homocysteine >10 microM), respectively. Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, electron microscopy of thoracic aorta and serum concentration of nitriteitrate. The expression of messenger RNA for p22phox and eNOS was assessed by reverse transcription-polymerase chain reaction. Serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion were estimated to assess oxidative stress. DAQ B1 (5 mg kg(-1), p.o.) or atorvastatin (30 mg kg(-1), p.o.) in diabetic and hyperhomocysteinemic rats significantly reduced serum glucose and homocysteine concentration. DAQ B1 or atorvastatin markedly improved acetylcholine-induced endothelium-dependent relaxation, vascular endothelial lining, serum nitriteitrate concentration and serum TBARS in diabetic and hyperhomocysteinemic rats. However, this ameliorative effect of DAQ B1 has been prevented by L-NAME (25 mg kg(-1), i.p.), an inhibitor of eNOS. Therefore, it may be concluded that DAQ B1-induced activation of Akt may activate eNOS and consequently reduce oxidative stress to improve vascular endothelial dysfunction.
机译：这项研究旨在研究Akt激活剂去甲基甾烷醌B1（DAQ B1）在糖尿病（DM）和高同型半胱氨酸血症（HHcy）诱导的血管内皮功能障碍中的作用。大鼠服用链脲佐菌素（55 mg kg（-1），iv）和蛋氨酸（1.7％w / w，po，4周）产生DM（血清葡萄糖> 140 mg dl（-1））和HHcy（血清高半胱氨酸> 10 microM）。使用分离的主动脉环制剂，胸主动脉的电子显微镜检查和亚硝酸盐/硝酸盐的血清浓度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的信使RNA的表达。估计血清硫代巴比妥酸反应性物质（TBARS）和主动脉超氧阴离子可评估氧化应激。糖尿病和高同型半胱氨酸血症大鼠的DAQ B1（5 mg kg（-1），p.o.）或阿托伐他汀（30 mg kg（-1），p.o.）显着降低了血清葡萄糖和同型半胱氨酸的浓度。 DAQ B1或阿托伐他汀在糖尿病和高同型半胱氨酸血症大鼠中显着改善了乙酰胆碱诱导的内皮依赖性舒张，血管内皮层，血清亚硝酸盐/硝酸盐浓度和血清TBARS。但是，DAQ B1的这种改善作用已被eNOS抑制剂L-NAME（25 mg kg（-1），i.p.）阻止。因此，可以得出结论，DAQ B1诱导的Akt激活可以激活eNOS，从而降低氧化应激，从而改善血管内皮功能障碍。

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