Pramipexole Protects Against Traumatic Brain Injury-Induced Blood–Brain Barrier (BBB) Dysfunction

普拉克索 创伤性脑损伤 封堵器 血脑屏障 神经保护 药理学 医学 星形胶质细胞 紧密连接 神经科学 化学 内科学 心理学 中枢神经系统 帕金森病 疾病 生物化学 精神科
作者
Junping Huang,Huan Lan,Changji Xie,Chengcong Wei,Zhen Liu,Zhixi Huang,Zhiyu Zhou,Lei Chen
出处
期刊:Neurotoxicity Research [Springer Science+Business Media]
卷期号:40 (4): 1020-1028 被引量:9
标识
DOI:10.1007/s12640-022-00495-6
摘要

Traumatic brain injury (TBI) is a severe disease of brain damage accompanied by blood–brain barrier (BBB) dysfunction. The BBB is composed of brain microvascular endothelial cells (BMECs), astrocyte terminus, pericytes, and a basement membrane. Tight junction proteins expressed by BMECs play important roles in preserving BBB integrity. Pramipexole is a selective dopamine agonist applied for treating Parkinson’s disease and has been recently claimed with neuroprotective capacity. This study will further explore the impact of Pramipexole on tight junctions and BBB integrity to provide the potential treatment strategy for TBI-induced BBB damage. The TBI model was established in mice and was identified by the promoted brain water content, declined Garcia scores, reduced latency of the rotarod test, aggravated pathological changes in the brain cortex, and excessively released inflammatory factors. After treatment with Pramipexole, the neurofunctional deficits, behavioral disability, and aggravated pathological changes were dramatically reversed, accompanied by the alleviated BBB permeability, and upregulated occludin, an important tight junction protein. TBI model cells were established by the scratching bEnd.3 cells method. Cells were stimulated with 10 and 20 μM Pramipexole, followed by exposure to TBI. Increased fluorescence intensity of FITC-dextran, reduced value of TEER, and downregulated occludin and KLF2 were observed in TBI-exposed cells, all of which were greatly reversed by 10 and 20 μM Pramipexole. Furthermore, in KLF2-silenced bEnd.3 cells, the protective ability of Pramipexole against endothelial permeability and the expression level of occludin were dramatically abolished. Collectively, our results suggest that Pramipexole protected against TBI-induced BBB dysfunction by mediating KLF2.
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