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首页> 外文期刊>American Journal of Physiology >Possible usefulness of apocynin, an NADPH oxidase inhibitor, for nitrate tolerance: prevention of NO donor-induced endothelial cell abnormalities.
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Possible usefulness of apocynin, an NADPH oxidase inhibitor, for nitrate tolerance: prevention of NO donor-induced endothelial cell abnormalities.

机译：NADPH氧化酶抑制剂Apocynin可能对硝酸盐耐受性有用：预防NO供体诱导的内皮细胞异常。

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The long-term benefits of nitroglycerin therapy are limited by tolerance development. Understanding the precise nature of mechanisms underlying nitroglycerin-induced endothelial cell dysfunction may provide new strategies to prevent tolerance development. In this line, we tested interventions to prevent endothelial dysfunction in the setting of nitrate tolerance. When bovine aortic endothelial cells (BAECs) were continuously treated with nitric oxide (NO) donors, including nitroglycerin, over 2-3 days, basal production of nitrite and nitrate (NO(x)) was diminished. The diminished basal NO(x) levels were mitigated by intermittent treatment allowing an 8-h daily nitrate-free interval during the 2- to 3-day treatment period. Addition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin restored the basal levels of NO(x) that were decreased by continuous nitroglycerin treatment of BAECs. Apocynin caused significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase (eNOS) in BAECs given nitroglycerin continuously over the treatment period. Apocynin also reduced endothelial production of reactive oxygen species (ROS) after continuous nitroglycerin treatment. These results showed an essential similarity to the effects of a nitrate-free interval. Application of the NOS inhibitor N(omega)-nitro- l-arginine methyl ester caused a recovery effect on basal NO(x) and eNOS expression but was without effect on ROS levels in continuously NO donor-treated BAECs. In conclusion, the present study characterized abnormal features and functions of endothelial cells following continuous NO donor application. We suggest that inhibition of NADPH oxidase, by preventing NO donor-induced endothelial dysfunction, may represent a potential therapeutic strategy that confers protection from nitrate tolerance development.
机译：硝酸甘油疗法的长期益处受到耐受性发展的限制。理解硝酸甘油诱导的内皮细胞功能障碍的机制的确切性质，可能提供防止耐受性发展的新策略。在这一方面，我们测试了预防硝酸盐耐受性设置中内皮功能障碍的干预措施。当牛主动脉内皮细胞（BAEC）用一氧化氮（NO）供体（包括硝酸甘油）连续处理2-3天时，亚硝酸盐和硝酸盐（NO（x））的基础产量就会减少。通过间歇治疗可以缓解基础NO（x）水平降低的情况，该间歇治疗可在2至3天的治疗期内每天进行8小时的无硝酸盐间隔。烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶抑制剂Apocynin的添加恢复了NO（x）的基础水平，该水平通过连续硝酸甘油处理BAEC降低了。在治疗期间连续给予硝化甘油的情况下，Apocynin引起BAEC中内皮型一氧化氮合酶（eNOS）mRNA和蛋白水平增加的显着改善。持续进行硝酸甘油处理后，阿波西宁还减少了内皮细胞产生的活性氧（ROS）。这些结果显示出与无硝酸盐间隔的效果基本相似。 NOS抑制剂N（ω）-硝基-1-精氨酸甲酯的应用对基础NO（x）和eNOS表达产生恢复作用，但对连续NO供体处理的BAEC中的ROS水平没有影响。总而言之，本研究的特征是连续应用NO供体后内皮细胞的异常特征和功能。我们建议通过阻止NO供体诱导的内皮功能障碍来抑制NADPH氧化酶，可能代表了一种潜在的治疗策略，可赋予其保护硝酸盐耐受性的能力。

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