Purpose

Restenosis is the main complication after percutaneous coronary intervention. The proliferation of new intima contributes to the process. In this study, we aimed to explore the effect of olmesartan on intimal thickening after balloon injury and possible mechanism.

Methods

Aortic endothelial denudation model was made by a 2F balloon catheter. Thirty-six rats were randomly allocated into three groups: Control (n = 12) Surgery (n = 12, received vascular balloon injury) and Olmesartan (n = 12, received 3 mg^.kg^-1.d^-1olmesartan after injury). Fourteen and 28 days after injury, HE staining was used to assess the aortic endothelial injury. Radioimmunological method was used to examine the level of angiotensin II (Ang II). Western blotting and reverse transcription polymerse chain reaction (RT-PCR) were employed to detect the protein and mRNA level of Apelin/APJ.

Results

After vascular balloon injury, the proliferation of vascular smooth muscle cells and the intimal thickening were increased. The mRNA and protein level of Ang II, AT1, Apelin and APJ mRNA were promoted by vascular balloon injury. Olmesartan decreased the proliferation of vascular smooth muscle cells and the intimal thickening. Olmesartan decreased the expression of Ang II and AT1, but further increased the expression of Apelin and APJ. Balloon injury also induced the activation of Extracellular signal-regulated kinase (ERK) signaling and olmesartan decreased the effect.

Conclusion

Olmesartan inhibits the intimal thickening through activating Apelin/APJ and inhibiting AngII-AT1 and ERK pathway.

中文翻译：

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奥美沙坦通过Apelin / APJ对球囊损伤后主动脉内膜增厚的影响。

目的

再狭窄是经皮冠状动脉介入治疗后的主要并发症。新内膜的扩散有助于该过程。在这项研究中，我们旨在探讨奥美沙坦对球囊损伤后内膜增厚的作用及其可能的机制。

方法

主动脉内皮剥脱模型由2F球囊导管制成。三十六个大鼠随机分为3组：对照（n = 12）手术（N = 12，接收到的血管内皮损伤）和奥美沙坦（N = 12，接受3毫克^。千克^-1。 d ^-1奥美沙坦损伤后） 。受伤后第十四天和第二十八天，HE染色用于评估主动脉内皮损伤。放射免疫法用于检查血管紧张素II（Ang II）的水平。采用蛋白质印迹和逆转录聚合酶链反应（RT-PCR）检测Apelin / APJ的蛋白质和mRNA水平。

结果

血管球囊损伤后，血管平滑肌细胞的增殖和内膜增厚增加。血管球囊损伤促进Ang II，AT1，Apelin和APJ mRNA的表达。奥美沙坦减少了血管平滑肌细胞的增殖和内膜增厚。奥美沙坦降低了Ang II和AT1的表达，但进一步提高了Apelin和APJ的表达。球囊损伤还诱导了细胞外信号调节激酶（ERK）信号的激活，奥美沙坦降低了该作用。

结论

奥美沙坦可通过激活Apelin / APJ并抑制AngII-AT1和ERK途径来抑制内膜增厚。