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目的研究NADPH氧化酶与血管壁活性氧(ROS)生成及再狭窄的关系。方法构建兔髂动脉2次损伤后再狭窄模型,逆转录-聚合酶链反应(RT-PCR)检测2次损伤后不同时段兔髂动脉NADPH氧化酶催化亚基gp91phox和p22phox mRNA表达的变化;原位杂交观察gp91phox和p22phox mRNA表达在血管壁的定位。结果gp91phox mRNA的表达在2次损伤后逐渐上升,在14 d(1．554±0．105)、28 d(1．444±0．360)达到峰值,与术后即刻组(0．572±0．018)比较,差异有统计学意义(P<0．01);p22phox mRNA的表达在2次损伤即刻(1．514±0．036)即处于高水平,术后1 d(0．832±0．059)略有下降后又逐渐升高,并在14 d(1．714±0．249)、28 d(1．564±0．151)达峰值。在2次损伤后,各时段血管壁gp91phox和p22phox mRNA均可见阳性表达,其表达主要位于新生内膜和外膜。结论NADPH氧化酶各个亚基在再狭窄过程中可能行使不同功能;氧化酶主要在新生内膜与外膜发挥作用。
Objective To study the relationship between NADPH oxidase and reactive oxygen species (ROS) generation and restenosis. Methods The rabbit model of iliac artery stenosis after secondary injury was established. The changes of mRNA expression of gp91phox and p22phox in the iliac artery were detected by reverse transcription-polymerase chain reaction (RT-PCR) at different time points. Hybridization was performed to observe the localization of gp91phox and p22phox mRNA in the vascular wall. Results The expression of gp91phox mRNA increased gradually after 2 times of injury and reached its peak at 14 days (1.554 ± 0.105) and 28 days (1.444 ± 0.360) 0.018), the difference was statistically significant (P <0.01); The expression of p22phox mRNA was high at 1.514 ± 0.036 immediately after injury, and at 1 day after operation (0.832 ± 0.059) and then increased gradually, reaching the peak at 14 days (1.714 ± 0.249) and 28 days (1.564 ± 0.151). After 2 times of injury, gp91phox and p22phox mRNA in blood vessel wall of each time period showed positive expression, which was mainly located in neointima and adventitia. Conclusion NADPH oxidase subunits may play different roles in the process of restenosis. Oxidase mainly plays a role in neointima and adventitia.