《中国康复理论与实践》

《中国康复理论与实践》 ›› 2004, Vol. 10 ›› Issue (09): 526-528.

• 基础研究 • 上一篇    下一篇

巴曲酶治疗糖尿病大鼠局灶性脑缺血再灌注损伤的实验研究

潘钰1,2; 丛琳3; 张朝东4   

  1. 1.北京博爱医院 北京市 100068;2.首都医科大学康复医学院 北京市 100068;3.中国医科大学第二临床学院神经内科 辽宁沈阳市 110001;4.中国医科大学第一临床学院神经内科 辽宁沈阳市 110001
  • 收稿日期:2004-07-05 出版日期:2004-09-25 发布日期:2004-09-25

Effect of Batroxobin on focal cerebral ischemia and reperfusion injury in streptozotocin-induced diabetic rats

PAN Yu, CONG Lin,ZHANG Chao-dong   

  1. Faculty of Rehabilitaion of Capital University of Medical Sciences, Beijing 100068,China
  • Received:2004-07-05 Published:2004-09-25 Online:2004-09-25

PDF (PC)

被引次数

17

摘要： 目的观察巴曲酶对糖尿病大鼠局灶性脑缺血再灌注损伤的影响及探讨巴曲酶是否对溶栓并发脑出血有保护作用及可能作用机制。方法腹腔注射链脲佐菌素建立糖尿病大鼠模型,血管内细丝栓堵大脑中动脉(MCA)2h后拔除线栓制作局灶脑缺血再灌注损伤模型,分别用巴曲酶、尿激酶以及两者联合治疗,同量注射生理盐水作为对照,观察MCA缺血再灌注后24h、48h各组大鼠脑梗死灶体积,脑出血发生及2—48h基质金属蛋白酶(MMP)-2、MMP-9的变化。结果各治疗组梗死灶体积及体积百分比比生理盐水组显著减小,各治疗组间无显著性差异;尿激酶组有5例发生脑出血,巴曲酶组无脑出血,联合应用巴曲酶与尿激酶组脑出血发生少于尿激酶组,但无显著性;巴曲酶组和联合应用巴曲酶与尿激酶组梗死灶周边MMP-2、MMP-9蛋白表达显著低于生理盐水组和尿激酶组。结论巴曲酶溶栓可使糖尿病大鼠局灶性脑缺血再灌注损伤梗死灶体积减小,减轻缺血再灌注损伤程度,无脑出血并发症,这一作用可能与巴曲酶抑制MMP-2和MMP-9的活化有关。

关键词: 巴曲酶, 局灶性脑缺血, 溶栓, 继发性脑出血, 糖尿病, 基质金属蛋白酶-2(MMP-2), 基质金属蛋白酶-9(MMP-9)

Abstract: ObjectiveTo observe the effect of Batroxobin and Urokinase on brain of diabetic rats following focal cerebral ischemia and reperfusion injury. To investigate the preventive mechanism of Batroxobin following focal cerebral ischemia and reperfusion injury in diabetic rats after thrombolysis therapy.MethodsDiabetic rat was induced by administrating streptozotocin intraperitoneally. Rat model of focal cerebral ischemia and reperfusion injury induced by intraluminal filament occlusion of middle cerebral artery(MCA) that removed 2h later was used. Batroxobin and Urokinase were administrated intravenously in different groups. Infarct volume,cerebral hemorrhage and matrix metalloproteinase (MMP)-2,MMP-9 were detected at 2h,24h,48h after ischemia and reperfusion injury.ResultsThe significant decrease of infarct volume were observed in Batroxobin and Urokinase groups. There were 5 rats observed cerebral hemorrhage in Urokinase group and no cerebral hemorrhage in Batroxobin group. The number of MMP-2 and MMP-9 positive cells in Batroxobin and Batroxobin Urokinase groups decreased compared with saline and Urokinase groups. ConclusionBatroxobin can decrease the infarct volume significantly without the complication of cerebral hemorrhage after ischemia and reperfusion injury in diabetic rats, which maybe relate to down regulation of the expression of MMP-2 and MMP-9.

Key words: Batroxobin, focal cerebral ischemia, thrombolysis, secondary cerebral hemorrhage, diabetes, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9(MMP-9)