Murakami J, Ohtani A, Murata S
Lead Optimization Research Laboratory, Tanabe Seiyaku Co., Ltd., Toda, Saitama, Japan.
Jpn J Pharmacol. 1997 Nov;75(3):291-4.
We have examined the effects of an inhibitor of plasminogen activator inhibitor-1 (PAI-1) production, (3E,4E)-3-benzylidene-4-(3,4,5-trimethoxy-benzylidene)pyrrol idine-2,5-dione (T-686), on lipopolysaccharide (LPS)-induced death in mice. Oral administration of T-686 (10 and 100 mg/kg/day) for 8 days prior to the LPS injection (35 mg/kg, i.v.) protected mice from the lethal effect of LPS in a dose-dependent fashion. Moreover, treatment with 100 mg/kg T-686 attenuated the increase in plasma PAI-1 activity and the decrease in AT-III activity induced by LPS. We conclude that T-686 can reduce the mortality of mice induced by LPS, which seems to be partially correlated with both hypercoagulation and hypofibrinolysis.
我们研究了纤溶酶原激活物抑制剂-1(PAI-1)生成抑制剂(3E,4E)-3-亚苄基-4-(3,4,5-三甲氧基-亚苄基)吡咯烷-2,5-二酮(T-686)对脂多糖(LPS)诱导的小鼠死亡的影响。在注射LPS(35 mg/kg,静脉注射)前8天口服给予T-686(10和100 mg/kg/天)可使小鼠免受LPS的致死作用,且呈剂量依赖性。此外,用100 mg/kg T-686治疗可减轻LPS诱导的血浆PAI-1活性增加和抗凝血酶III(AT-III)活性降低。我们得出结论,T-686可降低LPS诱导的小鼠死亡率,这似乎与高凝状态和纤维蛋白溶解功能减退均部分相关。