DDR1 may play a key role in destruction of the blood–brain barrier after cerebral ischemia–reperfusion

2015 ◽  
Vol 96 ◽  
pp. 14-19 ◽  
Author(s):  
Mingxia Zhu ◽  
Dong Xing ◽  
Zhihong Lu ◽  
Yanhong Fan ◽  
Wugang Hou ◽  
...  
2020 ◽  
Author(s):  
Jiaoyan Yu ◽  
Qingqing Liu ◽  
Xi Li ◽  
Mei Zhao ◽  
Ting Sun ◽  
...  

Abstract BackgroundIschemic stroke (IS) is a major neurological disease worldwide and is associated with extremely high morbidity and mortality. Oxymatrine (OMT) has neuroprotective properties and protects against IS. However, whether its protective effect involves the blood-brain barrier (BBB) integrity is unknown.MethodsHere, we used in vivo and in vitro models of IS to evaluate the protective effect of OMT and its mechanism with regard to the BBB. We assayed the role of OMT using neurological function scores and triphenyltetrazolium chloride, Nissl, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining.ResultsOMT significantly improved the neurological function and brain state and reduced BBB permeability in a mouse model of cerebral ischemia-reperfusion. Additionally, OMT improved the tight junction of bEend.3 cells under oxygen-glucose deprivation. Moreover, intracranial lentivirus injection-induced Cav-1 knockdown reduced the neuroprotective effects of OMT.ConclusionsOMT could improve I/R injury-induced damage to the BBB, and its effects may be related to the regulation of the Cav-1/MMP-9 signaling pathway. This suggests that OMT may offer effective protection against BBB injury after I/R.


2020 ◽  
Author(s):  
Jiaoyan Yu ◽  
Qingqing Lu ◽  
Xi Li ◽  
Mei Zhao ◽  
Ting Sun ◽  
...  

Abstract Ischemic stroke (IS) is a major neurological disease worldwide and is associated with extremely high morbidity and mortality. Oxymatrine (OMT) has neuroprotective properties and protects against IS. However, whether its protective effect involves the blood-brain barrier (BBB) integrity is unknown. In this study, we used in vivo and in vitro models of IS to evaluate the protective effect of OMT and its mechanism with regard to the BBB. Our results showed that OMT significantly improved the neurological function and brain state and reduced BBB permeability in a mouse model of cerebral ischemia-reperfusion. Additionally, OMT improved the tight junction of bEend.3 cells under oxygen-glucose deprivation. Moreover, intracranial lentivirus injection-induced Cav-1 knockdown reduced the neuroprotective effects of OMT. Our results indicated that OMT could improve cI/R injury-induced damage to the BBB, and its effects may be related to the regulation of the Cav-1/MMP-9 signaling pathway. This suggests that OMT may offer effective protection against BBB injury after cI/R.


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