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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >MRI EVALUATION OF BBB DISRUPTION AFTER ADJUVANT AcSDKP TREATMENT OF STROKE WITH tPA IN RAT
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MRI EVALUATION OF BBB DISRUPTION AFTER ADJUVANT AcSDKP TREATMENT OF STROKE WITH tPA IN RAT

机译：tPA佐剂佐治AcSDKP对大鼠卒中后BBB病变的MRI评价

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摘要

The primary limitation of thrombolytic treatment of ischemic stroke with tissue plasminogen activator (tPA) is the hemorrhagic risk. We tested AcSDKP (N-acetyl-serylaspartyl-lysyl-proline), as an auxiliary therapeutic agent, to reduce blood-brain barrier (BBB) disruption in a combination tPA thrombolytic treatment of stroke. Wistar rats subjected to embolic stroke were randomly assigned to either the tPA monotherapy group (n = 9) or combination of tPA and AcSDKP treatment group (n = 9) initiated at 4 h after ischemia. Magnetic resonance imaging (MRI) measurements were performed before and after the treatments. Immunohis-tochemical staining and measurements were performed to confirm MRI findings. Longitudinal MRI permeability measurements with gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA) demonstrated that combination treatment of acute embolic stroke with AcSDKP and tPA significantly reduced BBB leakage, compared to tPA monotherapy, at 3 and 6 days (18.3 ± 9.8 mm~3 vs 65.0 ± 21.0 mm~3, p < 0.001) after the onset of stroke, although BBB leakage was comparable between the two groups prior to the treatments (6.8 ± 4.4 mm~3 vs 4.3 ± 3.3 mm~3, p > 0.18). The substantial reduction of BBB leakage observed in the combination treatment group was closely associated with reduced ischemic lesions measured by T_2 maps (113.6 ± 24.9 mm~3 vs 188.1 ± 60.8 mm~3, p < 0.04 at 6 days). Histopathological analysis of the same population of rats showed that the combination treatment significantly reduced parenchymal fibrin deposition (0.063 ± 0.059 mm~2 vs 0.172 ± 0.103 mm~2, p < 0.03) and infarct volume (146.7 ± 35.9 mm~3 vs 199.3 ± 60.4 mm~3, p < 0.05) compared to the tPA monotherapy at 6 days after stroke. MRI provides biological insight into the therapeutic benefit of combination treatment of stroke with tPA and AcSDKP 4 h after onset, and demonstrates significantly improved cerebrovascular integrity with neuroprotective effects compared with tPA monotherapy.
机译：用组织纤溶酶原激活剂（tPA）进行的缺血性卒中溶栓治疗的主要局限性是出血风险。我们测试了作为辅助治疗剂的AcSDKP（N-乙酰基-赤藓糖氨酰-赖氨酰脯氨酸），以减少tPA溶栓治疗中风的血脑屏障（BBB）破坏。将发生栓塞性中风的Wistar大鼠随机分配至在缺血后4小时开始的tPA单药治疗组（n = 9）或tPA和AcSDKP治疗组的组合（n = 9）。在治疗之前和之后进行磁共振成像（MRI）测量。进行免疫组织化学染色和测量以确认MRI结果。用g-二亚乙基三胺五乙酸（Gd-DTPA）进行的纵向MRI渗透性测量表明，与tPA单一疗法相比，在3天和6天（18.3±9.8毫米〜中风发作后3 vs 65.0±21.0 mm〜3，p <0.001），尽管治疗前两组之间的BBB渗漏相当（6.8±4.4 mm〜3 vs 4.3±3.3 mm〜3，p> 0.18 ）。联合治疗组观察到的BBB渗漏的大量减少与通过T_2图测量的缺血性病变的减少密切相关（113.6±24.9 mm〜3与188.1±60.8 mm〜3，6天时p <0.04）。对相同大鼠群的组织病理学分析表明，联合治疗显着降低了实质性纤维蛋白沉积（0.063±0.059 mm〜2对0.172±0.103 mm〜2，p <0.03）和梗塞体积（146.7±35.9 mm〜3对199.3±）与卒中后第6天的tPA单一疗法相比，为60.4 mm〜3，p <0.05）。 MRI在发病后4 h提供tPA和AcSDKP联合治疗中风的治疗益处的生物学见解，并证明与tPA单药治疗相比，脑血管完整性显着改善，并具有神经保护作用。

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