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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Relationship among superoxide-related enzyme, PPARs, and endothelium-dependent relaxation in murine aortas previously organ-cultured in high-glucose conditions.
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Relationship among superoxide-related enzyme, PPARs, and endothelium-dependent relaxation in murine aortas previously organ-cultured in high-glucose conditions.

机译：先前在高葡萄糖条件下器官培养的小鼠主动脉中超氧化物相关酶，PPAR和内皮依赖性舒张之间的关系。

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摘要

The aim of the present study was to investigate the relationship among superoxide anion, peroxisome proliferator-activated receptors (PPARs), and endothelium-dependent relaxation in murine aortas organ-cultured in a high-glucose condition. Aortas organ-cultured with a high concentration of glucose (40 mmol/L, 20 h; HG group) exhibited the following characteristics (versus aortas cultured in serum-free medium): (i) significantly weaker relaxation to acetylcholine, but unchanged relaxation to SNP and unchanged contractions to norepinephrine and isotonic K+, (ii) significantly greater superoxide generation (indicated by the amount of nitroblue tetrazolium reduced, (iii) significantly higher protein expression levels of gp91phox, NAD(P)H oxidase subunits, and endothelial NO synthase, (iv) significantly lower protein expression level of Mn-superoxide dismutase (SOD), and (v) markedly greater reduction in the protein expression of PPARgamma than in that of PPARalpha. The HG-induced impairment of endothelium-dependent relaxation was prevented by cotreatment with tempol (a SOD mimetic). These results suggest that in the mouse aorta, exposure to high glucose levels may lead to an excessive generation of superoxide via increased gp91phox and decreased Mn-SOD protein expression and that this may in turn trigger an impairment of endothelium-dependent relaxation. Moreover, such protein changes in gp91phox and Mn-SOD may be secondary to a decreased expression of PPARgamma protein.
机译：本研究的目的是研究高糖条件下器官培养的小鼠主动脉中超氧阴离子，过氧化物酶体增殖物激活受体（PPAR）和内皮依赖性舒张之间的关系。用高浓度葡萄糖（40 mmol / L，20 h; HG组）进行器官培养的主动脉显示出以下特征（与在无血清培养基中培养的主动脉相比）：（i）对乙酰胆碱的松弛作用明显弱，但对乙酰胆碱的松弛作用不变SNP和不变的去甲肾上腺素和等渗K +的收缩，（ii）超氧化物的产生显着增加（由硝基蓝四唑的减少表示，（iii）gp91phox，NAD（P）H氧化酶亚基和内皮一氧化氮合酶的蛋白表达水平显着提高，（iv）Mn-超氧化物歧化酶（SOD）的蛋白表达水平明显降低，并且（v）PPARgamma的蛋白表达降低幅度明显大于PPARalpha，通过HG预防了HG诱导的内皮依赖性舒张损伤结果表明，在小鼠主动脉中，暴露于高葡萄糖水平可能会通过增加g导致过量产生超氧化物。 p91phox和Mn-SOD蛋白表达降低，进而可能触发内皮依赖性舒张功能受损。此外，gp91phox和Mn-SOD中的这种蛋白质变化可能是PPARgamma蛋白表达降低的原因。

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