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The effect of high glucose on NO and O-2(-) through endothelial GTPCH1 and NADPH oxidase

机译：高糖通过内皮GTPCH1和NADPH氧化酶对NO和O-2（-）的影响

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Although endothelial dysfunction deteriorates diabetic angiopathy, the mechanisms are obscure. We revealed that high glucose augmented eNOS through stimulation of eNOS mRNA in cultured BAECs. NO was decreased and O-2(-) was increased simultaneously. NOS inhibitor, inhibited O-2(-) release, so did NADPH oxidase inhibitor. The effects were synergistic. Both intracellular BH4 level and GTPCH1 activity were decreased by high glucose, in line with decrease of GTPCH1 mRNA. HMG-CoA, reductase inhibitor, atorvastatin increased GTPCH1 mRNA and activity, and BH4 level. Conclusively, high glucose leads to eNOS dysfunction by inhibiting BH4 synthesis and atorvastatin stimulate BH4 synthesis directly, and it may work as atherogenic process. (C) 2004 Elsevier Inc. All rights reserved.
机译：尽管内皮功能障碍使糖尿病性血管病恶化，但其机制尚不清楚。我们发现高糖通过刺激培养的BAECs中的eNOS mRNA增强了eNOS。 NO减少而O-2（-）同时增加。 NOS抑制剂抑制O-2（-）的释放，NADPH氧化酶抑制剂也是如此。效果是协同的。高糖降低了细胞内BH4水平和GTPCH1活性，这与GTPCH1 mRNA的降低相一致。 HMG-CoA，还原酶抑制剂，阿托伐他汀可增加GTPCH1 mRNA和活性以及BH4水平。结论是，高血糖会通过抑制BH4合成而导致eNOS功能障碍，而阿托伐他汀直接刺激BH4合成，并且可能起到动脉粥样硬化的作用。 （C）2004 Elsevier Inc.保留所有权利。

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