2005Chinese Journal of Cenebrovascular DiseasesRequires access

Experimental study of the neuroprotective effect of defibrase on focal ischemic-reperfusion injury of the brain in rats

Zhenpei Su

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Abstract

Objective To study the neuroprotective effect of defibrase on focal ischemic-reperfusion ingury of the brain in rats. Methods With stroke-prone renovascular hypertensive rats subjected to middle cerebral artery occlusion (MCAO)reperfusion injury of the brain, defibrase was injected intravenously in treatment groups, whereas the control groups received only normal saline, then was evaluated with neurological functions score 9 rats were killed at 3, 6, 24 hours after reperfusion for MCAO 3h and 6h respectively (8 sham-operated control group rats). Infarction size was measured by 2,3,5-triphenyltetrazolium chloride (TTC)staining and pathological changes was observed by HE staining, and immunohistochemistry was used to detected express of urokinase-type plasminogen activator(uPA)and plasminogen activator inhibitor-1(PAI-1).~Results In the treatment groups, the neurological function scores, infarction size, express of PAI-1 (gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3h and 6h respectively) and incidence of cerebral hemorrage decreased, whereas express of uPA gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3 h and 6 h respectively:1.240 ± 0.027、1.9 ± 1.1、12 ± 5、2.3 ± 1.2、6.4 ± 2.2 and 20 ± 7, in the control groups respectively: 1.320 ± 0.043、2.2 ± 1.0、16 ± 7、3.8 ± 1.6、8.3 ± 3.7 and 24 ± 10 increased significantly, as compared with control groups. ~Conclusion Defibrase can alleviate reperfusion injury of focal cerebral ischemia by reducing the degradative effect of uPA on the basement membrane of microvessels and extracellular mesenchyma around the infarction focus

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Objective To study the neuroprotective effect of defibrase on focal ischemic-reperfusion ingury of the brain in rats. Methods With stroke-prone renovascular hypertensive rats subjected to middle cerebral artery occlusion (MCAO)reperfusion injury of the brain, defibrase was injected intravenously in treatment groups, whereas the control groups received only normal saline, then was evaluated with neurological functions score 9 rats were killed at 3, 6, 24 hours after reperfusion for MCAO 3h and 6h respectively (8 sham-operated control group rats). Infarction size was measured by 2,3,5-triphenyltetrazolium chloride (TTC)staining and pathological changes was observed by HE staining, and immunohistochemistry was used to detected express of urokinase-type plasminogen activator(uPA)and plasminogen activator inhibitor-1(PAI-1).~Results In the treatment groups, the neurological function scores, infarction size, express of PAI-1 (gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3h and 6h respectively) and incidence of cerebral hemorrage decreased, whereas express of uPA gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3 h and 6 h respectively:1.240 ± 0.027、1.9 ± 1.1、12 ± 5、2.3 ± 1.2、6.4 ± 2.2 and 20 ± 7, in the control groups respectively: 1.320 ± 0.043、2.2 ± 1.0、16 ± 7、3.8 ± 1.6、8.3 ± 3.7 and 24 ± 10 increased significantly, as compared with control groups. ~Conclusion Defibrase can alleviate reperfusion injury of focal cerebral ischemia by reducing the degradative effect of uPA on the basement membrane of microvessels and extracellular mesenchyma around the infarction focus

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Available abstract

Objective To study the neuroprotective effect of defibrase on focal ischemic-reperfusion ingury of the brain in rats. Methods With stroke-prone renovascular hypertensive rats subjected to middle cerebral artery occlusion (MCAO)reperfusion injury of the brain, defibrase was injected intravenously in treatment groups, whereas the control groups received only normal saline, then was evaluated with neurological functions score 9 rats were killed at 3, 6, 24 hours after reperfusion for MCAO 3h and 6h respectively (8 sham-operated control group rats). Infarction size was measured by 2,3,5-triphenyltetrazolium chloride (TTC)staining and pathological changes was observed by HE staining, and immunohistochemistry was used to detected express of urokinase-type plasminogen activator(uPA)and plasminogen activator inhibitor-1(PAI-1).~Results In the treatment groups, the neurological function scores, infarction size, express of PAI-1 (gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3h and 6h respectively) and incidence of cerebral hemorrage decreased, whereas express of uPA gray scale value in treatment groups at 3, 6, 24 hours after reperfusion at MCAO 3 h and 6 h respectively:1.240 ± 0.027、1.9 ± 1.1、12 ± 5、2.3 ± 1.2、6.4 ± 2.2 and 20 ± 7, in the control groups respectively: 1.320 ± 0.043、2.2 ± 1.0、16 ± 7、3.8 ± 1.6、8.3 ± 3.7 and 24 ± 10 increased significantly, as compared with control groups. ~Conclusion Defibrase can alleviate reperfusion injury of focal cerebral ischemia by reducing the degradative effect of uPA on the basement membrane of microvessels and extracellular mesenchyma around the infarction focus

Key concepts: Medicine, Neuroprotection, Plasminogen activator, Ischemia, Reperfusion injury, Urokinase, Cerebral infarction, Tissue plasminogen activator

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