Kusama H, Kikuchi S, Tazawa S, Katsuno K, Baba Y, Zhai Y L, Nikaido T, Fujii S
Discovery Research Laboratories, Kissei Pharmaceutical Co. Ltd., Minamiazumi, Nagano, Japan.
Atherosclerosis. 1999 Apr;143(2):307-13. doi: 10.1016/s0021-9150(98)00308-6.
Restenosis after percutaneous transluminal coronary angioplasty (PTCA) occurs due to vascular smooth muscle cell proliferation and migration. Recently, tranilast, an anti-allergic drug, has been used for the prevention of restenosis after PTCA. To determine the molecular mechanism involved, the effect of tranilast on the proliferation of human coronary smooth muscle cells (SMCs) was investigated. Tranilast arrested the proliferation of human coronary SMCs at the G0/G1 phase of the cell cycle. In association with this inhibitory effect, tranilast increased p21waf1 and p53 tumor suppressor factor, and decreased cyclin-dependent kinase 2 (CDK2) activity. These results suggest that tranilast inhibits the proliferation of human coronary SMCs during restenosis after PTCA via an induction of p21waf1 and p53. Tranilast may thus allow us to prevent restenosis after PTCA by interfering with this mechanism.
经皮腔内冠状动脉成形术（PTCA）后再狭窄是由血管平滑肌细胞增殖和迁移引起的。最近，一种抗过敏药物曲尼司特已被用于预防PTCA后的再狭窄。为了确定其中涉及的分子机制，研究了曲尼司特对人冠状动脉平滑肌细胞（SMC）增殖的影响。曲尼司特使处于细胞周期G0/G1期的人冠状动脉SMC增殖停滞。伴随着这种抑制作用，曲尼司特增加了p21waf1和p53肿瘤抑制因子，并降低了细胞周期蛋白依赖性激酶2（CDK2）的活性。这些结果表明，曲尼司特通过诱导p21waf1和p53来抑制PTCA后再狭窄期间人冠状动脉SMC的增殖。因此，曲尼司特可能使我们通过干扰这一机制来预防PTCA后的再狭窄。
