高剂量他类药物治疗减少了急性心肌梗塞后循环的Dickkopf-1
Thor Ueland1, Noreen Butt2, Tove Lekva3
1Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; K. G. Jebsen Thrombosis Research and Expertise Center, University of Tromsø, Tromsø, Norway.
高剂量的罗斯瓦斯塔丁在ST段升高心肌梗塞 (STEMI) 患者中显著降低了Dickkopf-1 (DKK-1) 水平,长达两个月. 达丁类药物治疗也在内皮细胞中剂量依赖地降低了DKK-1.
科学领域:
- 心血管医学 心血管医学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 迪克科普夫 (DKK) 家族的葡萄糖蛋白影响Wnt信号,并可能影响斑块的稳定性.
- 达丁类药物对心肌梗塞 (MI) 患者的DKK水平的影响尚不清楚.
研究的目的:
- 研究在急性ST段升高心肌梗塞 (STEMI) 患者中,他类药物对血Dickkopf-1 (DKK-1) 和DKK-3的调节.
- 评估他类药物在人静脉内皮细胞 (HUVECs) 中对DKK-1表达的体外影响.
主要方法:
- 血DKK-1和DKK-3在皮肤冠状动脉干预 (PCI) 之前和之后测量STEMI患者,使用高剂量罗斯瓦斯塔丁 (40 mg) 或中剂量西姆瓦斯塔丁 (20 mg).
- 通过他类药物对DKK-1调节进行了体外HUVEC评估.
主要成果:
- 高剂量的罗斯瓦斯塔丁导致DKK-1水平持续下降,直到STEMI后两个月.
- 在用他类药物治疗的HUVEC中观察到DKK-1mRNA和蛋白质的剂量依赖性减少.
- 在两组中,DKK-3水平在STEMI后暂时增加,但恢复到基线.
结论:
- 高剂量他类药物治疗 (40毫克罗斯瓦斯塔丁) 可能在STEMI患者中持续下调DKK-1.
- 达丁类药物治疗对内皮细胞中DKK-1表达有直接的抑制作用.
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