Inhibition of platelet aggregation by polyaspartoyl L-arginine and its mechanism

• 来源期刊: 中国药理学报（英文版）
• 学科: 医学
• 关键词: platelet aggregation bleeding time platelet adhesiveness polyaspartoyl L-arginine nitric oxide cyclic AMP Thromboxane B2 6-ketoprostaglandin F1 alpha
• 年，卷（期）: 2004,（4）
• 页码范围: 469-473
• 页数: 5页
• 分类号: R9
• 语种: 英文

摘要

AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born's method;bleeding time was determined using tail's bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess' method; and cAMP, thromboxane B2 (TXB2) and 6-keto-PGF1a were assessed with commercial kits. RESULTS: The inhibition by PDR (15-60 mg/kg ig or 10 mg/kg iv) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 20 min after iv injection for rats (P<0.01), and its (15 mg/kg, ig) inhibition of ADP-induced platelet aggregation for rabbits during 6 h after administration were observed. PDR (15-60 mg/kg) prolonged the bleeding time of mice (P<0.05) and (30 mg/kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2 or 6-keto-PGF1a in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism possibly related to increasing NO generation.