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首页> 外文期刊>Life sciences >Buthionine sulfoximine causes endothelium dependent hyper-relaxation and hypoadiponectinemia.
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Buthionine sulfoximine causes endothelium dependent hyper-relaxation and hypoadiponectinemia.

机译：丁硫氨酸亚砜亚胺引起内皮依赖性的过度松弛和低脂联素血症。

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A close relationship between oxidative stress, endothelial dysfunction, and hypoadiponectinemia has been observed. The present study was performed to investigate how glutathione depletion via buthionine sulfoximine (BSO) administration affects endothelial function and adiponectin levels in rats. Acetylcholine (Ach)-induced vasodilation was significantly enhanced in BSO-treated rats, compared with control rats. This was completely abolished by L-NAME, and Ach-induced vasodilation was not observed in the aorta without endothelium. These results suggest that Ach-induced hyper-relaxation of the aorta in BSO-treated rats is completely dependent on the presence of endothelium and mediated by changes in eNOS activity. Catalase significantly inhibited this relaxation to Ach and no effect of catalase on sodium nitroprusside-induced relaxation of the aorta without endothelium was observed in BSO-treated rats. Thus, hyper-relaxation of the aorta in BSO-treated rats is likely caused by H2O2 in addition to NO produced by the endothelium via an eNOS-dependent mechanism. Hypoadiponectinemia and decreased levels of adiponectin mRNA in adipose tissue were observed in BSO-treated rats. Protein expression of eNOS and SODs (SOD-1 and SOD-2) in the aorta was increased and plasma NOx levels were decreased in BSO-treated rats. Our results suggest that oxidative stress induced by BSO causes eNOS uncoupling and hyper-relaxation by producing H2O2, and that BSO-induced oxidative stress causes hypoadiponectinemia, probably by increasing H2O2 production in adipose tissue.
机译：氧化应激，内皮功能障碍和低脂联素血症之间存在密切的关系。进行本研究以研究通过丁硫氨酸亚砜亚胺（BSO）给药引起的谷胱甘肽耗竭如何影响大鼠的内皮功能和脂联素水平。与对照组相比，在BSO治疗的大鼠中乙酰胆碱（Ach）诱导的血管舒张作用显着增强。 L-NAME完全消除了这种情况，并且在没有内皮的主动脉中未观察到Ach诱导的血管舒张。这些结果表明，在BSO处理的大鼠中，Ach诱导的主动脉过度松弛完全取决于内皮细胞的存在，并由eNOS活性的变化介导。过氧化氢酶显着抑制了这种对Ach的松弛，在用BSO处理的大鼠中未观察到过氧化氢酶对硝普钠诱导的无内皮主动脉松弛的作用。因此，除了通过内皮细胞通过eNOS依赖性机制产生的NO之外，BSO处理的大鼠中主动脉的过度松弛还可能由H2O2引起。在BSO处理的大鼠中观察到低脂联素血症和脂肪组织中脂连素mRNA水平降低。在BSO处理的大鼠中，主动脉中eNOS和SOD（SOD-1和SOD-2）的蛋白质表达增加，血浆NOx含量降低。我们的研究结果表明，BSO诱导的氧化应激通过产生H2O2导致eNOS解偶联和过度松弛，而BSO诱导的氧化应激可能导致脂联素血症，可能是通过增加脂肪组织中的H2O2产生。

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