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目的:探讨在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMCs)NOX1基因表达增加中线粒体所起的作用。方法:体外培养大鼠主动脉VSMCs,用线粒体呼吸链的抑制剂阻断线粒体的作用,用荧光实时定量PCR检测NOX1基因表达的量。结果:AngⅡ能够诱导NOX1基因的表达增加,线粒体呼吸链的抑制剂能够抑制上述这一作用。结论:在大鼠的VSMCs中,AngⅡ诱导NOX1的增加通过线粒体呼吸的作用。
AIM: To investigate the role of mitochondria in the increase of NOX1 gene expression induced by angiotensin Ⅱ (AngⅡ) in vascular smooth muscle cells (VSMCs). Methods: VSMCs of rat aorta were cultured in vitro. Mitochondria were blocked by inhibitors of mitochondrial respiratory chain. The expression of NOX1 gene was detected by real-time fluorescence quantitative PCR. Results: AngⅡ could induce the increase of NOX1 gene expression. Inhibitors of mitochondrial respiratory chain could inhibit this effect. CONCLUSION: Ang II induces an increase in NOX1 through mitochondrial respiration in rat VSMCs.