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巴曲酶(去纤酶)对大鼠的去纤维蛋白原作用及巴曲酶处理大鼠血浆对人血管平滑肌细胞体外迁移的抑制作用

Defibrinogenating effect of batroxobin (Defibrase) in rats and inhibition of migration of human vascular smooth muscle cells by the plasma of batroxobin-treated rats in vitro.

作者信息

Wang D S, Hanamoto M, Fang F, Ohba M, Ishii M, Kimura F, Higaki E, Senga H

机构信息

Ome Research Laboratories, Tobishi Pharmaceutical Co., Ltd. 7-1, 1-chome, Suehiro-cho, Ome-shi, Tokyo 198-0025, Japan.

出版信息

Atherosclerosis. 2001 May;156(1):73-80. doi: 10.1016/s0021-9150(00)00628-6.

Abstract

The defibrinogenating effect of batroxobin (Defibrase) in male Wistar rats and the inhibitory effects of the plasma of batroxobin-treated rats on the migration of human vascular smooth muscle cells (SMCs) were investigated in vitro. At 1 h after a single intravenous injection of 3.0, 10.0 or 30.0 BU/kg batroxobin (ten rats in each group), the fibrinogen levels in the plasma of the rats decreased to 88.3, 66.2 and 16.5%, respectively, of that in the plasma of control saline-treated rats (261.0+/-26.7 mg/dl). When the plasma from the batroxobin-treated rats was added to Dulbecco's modified Eagle's medium at a concentration of 0.2% for a vascular SMC migration assay and incubated in a modified Boyden's chamber system at 37 degrees C for 24 h, significant inhibitory effects on vascular SMC migration were observed in the 10.0 (P<0.05) and 30.0 BU/kg (P<0.01) batroxobin-treated rats. The plasma of batroxobin-treated rats as well as standard rat fibrinogen induced vascular SMC migration in a fibrinogen content-dependent manner except the plasma of the 30.0 BU/kg batroxobin-treated rats. Moreover, the rat serum (0.1 approximately 5.0%) did not show any activity on vascular SMC migration in the present experimental system. These results indicate that the plasma fibrinogen significantly influences vascular SMC migration, and that the inhibitory effect of the plasma of batroxobin-treated rats on vascular SMC migration is related to the defibrinogenating action of batroxobin in vivo.

摘要

研究了巴曲酶(去纤酶)对雄性Wistar大鼠的去纤维蛋白原作用,以及巴曲酶处理大鼠的血浆对人血管平滑肌细胞(SMC)迁移的抑制作用。单次静脉注射3.0、10.0或30.0 BU/kg巴曲酶后1小时(每组10只大鼠),大鼠血浆中的纤维蛋白原水平分别降至生理盐水处理的对照大鼠血浆(261.0±26.7 mg/dl)的88.3%、66.2%和16.5%。当将巴曲酶处理大鼠的血浆以0.2%的浓度添加到杜尔贝科改良伊格尔培养基中用于血管SMC迁移试验,并在改良的博伊登室系统中于37℃孵育24小时时,在10.0(P<0.05)和30.0 BU/kg(P<0.01)巴曲酶处理的大鼠中观察到对血管SMC迁移有显著抑制作用。除30.0 BU/kg巴曲酶处理大鼠的血浆外,巴曲酶处理大鼠的血浆以及标准大鼠纤维蛋白原均以纤维蛋白原含量依赖的方式诱导血管SMC迁移。此外,在本实验系统中,大鼠血清(0.1%至5.0%)对血管SMC迁移未显示任何活性。这些结果表明,血浆纤维蛋白原显著影响血管SMC迁移,且巴曲酶处理大鼠的血浆对血管SMC迁移的抑制作用与巴曲酶在体内的去纤维蛋白原作用有关。

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