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Tongxinluo Enhances Neurogenesis and Angiogenesis in Peri-Infarct Area and Subventricular Zone and Promotes Functional Recovery after Focal Cerebral Ischemic Infarction in Hypertensive Rats

机译:通心络增强高血压大鼠局灶性脑梗死后脑梗死区和脑室下区的神经发生和血管新生促进功能恢复

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摘要

Background. Tongxinluo is a traditional Chinese medicine compound with the potential to promote the neuronal functional recovery in cerebral ischemic infarction. Objective. This study aimed to disclose whether tongxinluo promotes neurological functional recovery and neurogenesis and angiogenesis in the infarcted area and SVZ after cerebral ischemic infarction in hypertensive rats. Methods. The ischemic model was prepared by distal middle cerebral artery occlusion (MCAO) in hypertensive rats. Tongxinluo was administrated 24 h after MCAO and lasted for 3, 7, or 14 days. Behavioral tests were performed to evaluate the protection of tongxinluo. Immunochemical staining was applied on brain tissue to evaluate the effects of tongxinluo on neurogenesis and vascularization in the MCAO model rats. Results. Postinjury administration of tongxinluo ameliorated the neuronal function deficit in the MCAO model rats. As evidenced by the immunochemical staining, BrdU+/DCX+, BrdU+estin+, and BrdU+ vascular endothelial cells were promoted to proliferate in SVZ after tongxinluo administration. The matured neurons stained by NeuN and vascularization by laminin staining were observed after tongxinluo administration in the peri-infarct area. Conclusion. Tongxinluo postischemia administration could ameliorate the neurological function deficit in the model rats. Possible mechanisms are related to neurogenesis and angiogenesis in the peri-infarct area and SVZ.
机译:背景。通心络是一种中药复方,具有促进脑缺血性脑梗死神经元功能恢复的潜力。目的。这项研究旨在揭示通心络是否促进高血压大鼠脑缺血性梗死后梗死区和SVZ的神经功能恢复以及神经发生和血管生成。方法。通过高血压大鼠大脑中动脉远端闭塞(MCAO)制备缺血模型。通心络在MCAO后24小时给药,持续3、7或14天。进行行为测试以评估通心络的保护作用。将免疫化学染色应用于脑组织,以评估通心络对MCAO模型大鼠神经发生和血管形成的影响。结果。通心络的损伤后给药改善了MCAO模型大鼠的神经元功能缺陷。免疫化学染色证明,BrdU + / DCX + ,BrdU + / nestin + 和BrdU <通心络给药后,sup> + 血管内皮细胞在SVZ中增殖。通心络给药后在梗死周围区域观察到了被NeuN染色的成熟神经元和层粘连蛋白染色的血管形成。结论。通心络缺血后给药可改善模型大鼠的神经功能缺损。可能的机制与梗死周围区域和SVZ的神经发生和血管生成有关。

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