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环氧化酶-2抑制剂可减轻血管紧张素II诱导的大鼠氧化应激、高血压和心脏肥大。

Cyclooxygenase-2 inhibitors attenuate angiotensin II-induced oxidative stress, hypertension, and cardiac hypertrophy in rats.

作者信息

Wu Rong, Laplante Marc-André, de Champlain Jacques

机构信息

Department of Physiology, University of Montreal, Montréal, Québec, Canada.

出版信息

Hypertension. 2005 Jun;45(6):1139-44. doi: 10.1161/01.HYP.0000164572.92049.29. Epub 2005 Apr 25.

Abstract

Angiotensin II is an important oxidative stress mediator. Our previous studies have indicated that the potent antioxidative properties of acetylsalicylic acid play an important role in its cardiovascular protective effects. There are some ongoing controversies concerning the use of selective cyclooxygenase-2 inhibitors in cardiovascular disease. The aim of this study was to determine whether the cyclooxygenase-2 selective inhibitors rofecoxib and nimesulide possess antioxidative and cardiovascular protective effects against angiotensin II. Chronic subcutaneous angiotensin II infusion increased cardiovascular but not colonic tissue superoxide production, heart/body weight ratio, and blood pressure. Moreover, angiotensin II selectively increased cardiac cyclooxygenase-2 but not cyclooxygenase-1 expression, which was totally prevented by acetylsalicylic acid treatment. Similar to acetylsalicylic acid, rofecoxib or nimesulide treatments significantly attenuated angiotensin II-induced oxidative stress, hypertension, and cardiac NAD(P)H oxidase subunit p47(phox) expression. Rofecoxib also reduced cardiac hypertrophy. Treatment with nonselective anti-inflammatory drugs ibuprofen, indomethacin, or salicylic acid did not show any effect on angiotensin II-induced superoxide production, hypertension, or cardiac hypertrophy. Although acetylsalicylic acid and salicylic acid inhibited angiotensin II-induced nuclear factor kappaB (NF-kappaB) activation, nimesulide did not modify NF-kappaB activation. In conclusion, cyclooxygenase-2 pathway is implicated in angiotensin II-induced oxidative stress and deleterious cardiovascular changes. Rofecoxib and nimesulide produced significant antioxidative effect by reducing NAD(P)H oxidase-dependent superoxide generation. These effects seem to be independent of NF-kappaB inhibition.

摘要

血管紧张素II是一种重要的氧化应激介质。我们之前的研究表明,乙酰水杨酸强大的抗氧化特性在其心血管保护作用中发挥着重要作用。关于选择性环氧化酶-2抑制剂在心血管疾病中的应用存在一些争议。本研究的目的是确定环氧化酶-2选择性抑制剂罗非昔布和尼美舒利是否具有针对血管紧张素II的抗氧化和心血管保护作用。慢性皮下输注血管紧张素II可增加心血管组织而非结肠组织的超氧化物生成、心脏/体重比和血压。此外,血管紧张素II选择性增加心脏环氧化酶-2的表达,但不增加环氧化酶-1的表达,乙酰水杨酸治疗可完全阻止这种情况。与乙酰水杨酸类似,罗非昔布或尼美舒利治疗可显著减轻血管紧张素II诱导的氧化应激、高血压和心脏烟酰胺腺嘌呤二核苷酸磷酸(NAD(P)H)氧化酶亚基p47(phox)的表达。罗非昔布还可减轻心脏肥大。使用非选择性抗炎药布洛芬、吲哚美辛或水杨酸治疗对血管紧张素II诱导的超氧化物生成、高血压或心脏肥大没有任何影响。虽然乙酰水杨酸和水杨酸可抑制血管紧张素II诱导的核因子κB(NF-κB)激活,但尼美舒利并未改变NF-κB的激活。总之,环氧化酶-2途径与血管紧张素II诱导的氧化应激和有害的心血管变化有关。罗非昔布和尼美舒利通过减少NAD(P)H氧化酶依赖性超氧化物生成产生显著的抗氧化作用。这些作用似乎与NF-κB抑制无关。

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