NADPH氧化酶Nox4调控非诺贝特的抗高血压心肌肥大效应

目的拟阐明NADPH氧化酶Nox4与非诺贝特抗高血压心肌肥大效应的关系。方法构建腹主动脉缩窄(abdominal aorta coarctation,AAC)诱导的高血压大鼠模型,观察非诺贝特对高血压大鼠左心室肥大的影响。结果非诺贝特可显著抑制AAC高血压大鼠左心室肥大。与假手术组比较,AAC组左心室中NADPH氧化酶Nox4蛋白和mRNA水平均显著增加;与AAC组比较,非诺贝特剂量依赖性降低AAC高血压大鼠左心室中NADPH氧化酶Nox4蛋白和mRNA水平。结论降低NADPH氧化酶Nox4表达可能是非诺贝特发挥抗高血压心肌肥大效应的重要机制。

NADPH Oxidase Nox4 Regulates the Protective Effect of Fenofribate Against Cardiac Hypertrophy

Aim To elucidate the relation between NADPH oxidase Nox4 and the protective effect of fenofribate against cardiac hypertrophy. Methods Abdominal aorta coarctation (AAC)-induced hypertensive rats were constructed to observe the effect of fenofribate on left ventricular hypertrophy. Results Fenofribate could inhibit left ventricular hypertrophy in AAC-induced hypertensive rats. Compared with sham group, the mRNA and protein levels of NADPH oxidase Nox4 were significantly elevated in left ventricular tissue of AAC group; compared with AAC group, fenofribate reduced the mRNA and protein levels of NADPH oxidase Nox4 in left ventricular tissue in a dose-dependent manner.Conclusion Reducing NADPH oxidase Nox4 expression could be a crucial mechanism of fenofribate against hypertension-induced cardiac hypertrophy. It will provide further theoretical and experimental support for fenofribate curing hypertension- induced myocardial hypertrophy.