Trapidil (Avantrin) is a coronary vasodilator agent. It was originally developed as a vasodilator and anti-platelet agent and has been used to treat patients with ischemic coronary heart, liver, and kidney disease.

Trapidil 在PDGF及其受体在蛋白水平上抑制自分泌回路，并显示出显著的抗增殖活性[1]。Trapidi l的添加量在100至400 μg/ml能显著减少由不同生长因子(FCS, PDGF-BB, bFGF, EGF)诱导的细胞增殖，尤其是对PDGF-BB刺激的Mesangial细胞(MC)生长抑制效果显著。Trapidil 作为一种抗血小板化合物，能抵抗多种聚集反应，比如胶原、ADP、花生四烯酸、PAF和钙离子载体的聚集。Trapidil 通过阻断血栓素A2的生物合成，拮抗其在受体水平的作用，并通过刺激前列环素的合成和释放发挥作用[2]。Trapidil在骨髓细胞和成骨细胞的共培养体系中强烈抑制成骨破骨细胞的形成，而不影响成骨细胞中受体活化剂NF-κB配体(RANKL)或骨保护素的表达。此外，Trapidil抑制 RANKL诱导成破骨细胞前体的形成。Trapidil减少RANKL诱导的核因子活化的T细胞和细胞质1(NFATc1)的表达。Trapidil 抑制磷酸二酯酶、血栓素A2和CD40信号，激活蛋白激酶A[3]。

Trapidil 是一种具有特定血小板源性生长因子（PDGF）抗性和抗增殖效果的抗血小板聚集化合物。在大鼠和兔子模型中，Trapidil 的抗血小板聚集活性经过气球血管成形术后可见效果[1]。在动物模型中，Trapidil对由白细胞介素-1诱导的破骨细胞形成和骨吸收有显著的抑制作用。腹腔注射Trapidil后，未观察到体重变化、腹泻、高烧和抽搐等异常症状[3]。

Cell viability was determined by Trypan blue dye exclusion test and LDH assay. Supernatants, collected from cells seeded in serum-free medium and exposed to the different mitogens and drugs tested, were centrifuged and LDH concentration determined. Supernatants obtained from sonicated cells were used as a positive control. Furthermore, to definitely exclude a cytotoxic effect of Trapidil on human MC, cells incubated for four days with and without the drug were challenged with fresh medium containing 10% FBS, and cell proliferation evaluated. (Only for Reference)