Kikuchi S, Umemura K, Kondo K, Nakashima M
Department of Pharmacology, Hamamatsu University School of Medicine, Japan.
Eur J Pharmacol. 1996 Jan 11;295(2-3):221-7. doi: 10.1016/0014-2999(95)00636-2.
Intimal thickening in the femoral artery of spontaneously hypertensive rats (SHR) was initiated by endothelial damage induced by the photochemical reaction between green light and systemic rose bengal. This model represents a non-mechanical method of producing vessel wall denudation. Neointima formation was assessed by calculating the cross-sectional area of intima, media and lumen, using computer analysis. Tranilast (30, 100 and 300 mg/kg, p.o.), administered 2 days prior to endothelial injury, reduced intimal area by 29, 62 and 87%, respectively, compared to that of vehicle-treated controls. In cultured SHR-derived vascular smooth muscle cells, tranilast produced concentration-dependent inhibition of mitogenesis, whether stimulated by platelet-derived growth factor, basic fibroblast growth factor, insulin-like growth factor or fetal bovine serum. These results suggest that tranilast may be effective in preventing coronary restenosis.
自发性高血压大鼠（SHR）股动脉内膜增厚是由绿光与全身注射孟加拉玫瑰红之间的光化学反应诱导的内皮损伤引发的。该模型代表了一种产生血管壁剥脱的非机械方法。通过计算机分析计算内膜、中膜和管腔的横截面积来评估新生内膜的形成。在内皮损伤前两天口服给予曲尼司特（30、100和300mg/kg），与给予赋形剂的对照组相比，内膜面积分别减少了29%、62%和87%。在培养的SHR来源的血管平滑肌细胞中，无论由血小板衍生生长因子、碱性成纤维细胞生长因子、胰岛素样生长因子还是胎牛血清刺激，曲尼司特都产生浓度依赖性的有丝分裂抑制作用。这些结果表明，曲尼司特可能对预防冠状动脉再狭窄有效。
