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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >2-(2-Benzofuranyl)-2-Imidazoline Mediates Neuroprotection by Regulating the Neurovascular Unit Integrity in a Rat Model of Focal Cerebral Ischemia
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2-(2-Benzofuranyl)-2-Imidazoline Mediates Neuroprotection by Regulating the Neurovascular Unit Integrity in a Rat Model of Focal Cerebral Ischemia

机译：2-（2-苯并呋喃基）-2-咪唑啉通过调节局灶性脑缺血大鼠模型中的神经血管单位完整性来介导神经保护作用

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Background: We showed previously that 2-(2-benzofuranyl)-2-imidazoline (2-BFI), a ligand to type 2 imidazoline receptor (I2R) exerts neuroprotective effects in ischemia stroke via an unknown mechanism. The present study was to investigate whether 2-BFI can protect the neurovascular unit (NVU) using a rat model of 90 min focal cerebral ischemia. Methods: Rats were randomly divided into three groups: thesham-operated group; the vehicle control group and the 2-BFI group which received 2-BFI (3 mg/kg) immediately after the start of middle cerebralartery occlusion (MCAO). Neurological deficit score, infarct size, apoptosis level, brain water content and Evans Blue extravasation were assessed at 24 h after stroke. Expressions of occludin and zonula occludens 1 (ZO-1), collagen IV, aquaporin-4 (AQP-4), matrix metalloproteinase-9 (MMP-9) and MMP-2 were assessed by Western blotting. Results: 2-BFI treatment was associated with significant improvement of neurological performance and decreased infarct volume at 24 h after stroke. Apoptosis level reduced significantly by 2-BFI compared to the vehicle group (34.3 +/- 5.4% vs 56.1 +/- 7.9%, p 0.05). Significant decreased of brain water content (79.5 +/- 2.6% vs 84.62 +/- 2%, p 0.05) and Evans Blue extravasation (1.2 +/- 0.5 vs 2.5 +/- 0.41 mu g/g, p 0.05) of ipsilateral hemisphere was observed in 2-BFI group compared to vehicle group. Expressions of occludin, ZO-1 and collagen IV were significantly higher while MMP-9 level significantly lower in 2-BFI group. AQP-4 and MMP-2 showed no difference between 2-BFI and the vehicle groups. Conclusions: These results suggest that the neuroprotective effects of 2-BFI in acute ischemic brain damage are at least partly due to the drug's ability to improve the functions of NVU.
机译：背景：以前显示，2-（2-苯并呋喃基）-2-咪唑啉（2-BFI），咪唑啉受体（I2R）的配体通过未知机制施加神经保护作用。本研究是研究2-BFI是否可以使用90分钟局灶性脑缺血的大鼠模型来保护神经血管单元（NVU）。方法：将大鼠随机分为三组：TheMam操作组;在中脑动脉闭塞（MCAO）开始后立即接受2-BFI（3mg / kg）的车辆对照组和2-BFI组。卒中后24小时评估神经缺陷分数，梗塞大小，凋亡水平，脑水含量和evans蓝外渗。通过蛋白质印迹评估紫外线和ZO-1），胶原蛋白IV，Aquaporin酶-9，基质金属蛋白酶-9（MMP-9）和MMP-2的表达式occludin和ZO-1），胶原蛋白IV，Aquaporine-4（MMP-9）和MMP-2。结果：2-BFI处理与显着改善神经性能的显着改善，卒中后24小时下降梗塞体积。与载体组相比，凋亡水平明显减少了2-BFI（34.3 +/- 5.4％Vs 56.1 +/- 7.9％，P <0.05）。脑含水量显着下降（79.5 +/- 2.6％Vs 84.62 +/- 2％，P <0.05）和EVANS蓝前进（1.2 +/- 0.5 Vs 2.5 +/-0.41μg/ g，p＆与载体组相比，在2-BFI组中观察到同侧半球0.05）。 occludin，ZO-1和胶原蛋白IV的表达显着提高，而2-BFI组MMP-9水平显着降低。 AQP-4和MMP-2在2-BFI和车辆组之间没有差异。结论：这些结果表明，2-BFI在急性缺血性脑损伤中的神经保护作用至少部分地是由于药物改善NVU功能的能力。

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