scholarly journals Thrombolytic activity of Cheonggukjang kinase on the recovery of brain damage in cerebral embolic stroke model

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Young‐Sun Song ◽  
Angela Melinda Anak Anthony Jalin ◽  
A Reum Kang ◽  
Chae Yeon Lee ◽  
Chung Mu Park ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoonhee Kim ◽  
Yoon Bum Lee ◽  
Seung Kuk Bae ◽  
Sung Suk Oh ◽  
Jong-ryul Choi

AbstractPhotochemical thrombosis is a method for the induction of ischemic stroke in the cerebral cortex. It can generate localized ischemic infarcts in the desired region; therefore, it has been actively employed in establishing an ischemic stroke animal model and in vivo assays of diagnostic and therapeutic techniques for stroke. To establish a rabbit ischemic stroke model and overcome the shortcoming of previous studies that were difficult to build a standardized photothrombotic rabbit model, we developed a photochemical thrombosis induction system that can produce consistent brain damage on a specific area. To verify the generation of photothrombotic brain damage using the system, longitudinal magnetic resonance imaging, 2,3,5-triphenyltetrazolium chloride staining, and histological staining were applied. These analytical methods have a high correlation for ischemic infarction and are appropriate for analyzing photothrombotic brain damage in the rabbit brain. The results indicated that the photothrombosis induction system has a main advantage of being accurately controlled a targeted region of photothrombosis and can produce cerebral hemisphere lesions on the target region of the rabbit brain. In conjugation with brain atlas, it can induce photochemical ischemic stroke locally in the part of the brain that is responsible for a particular brain function and the system can be used to develop animal models with degraded specific functions. Also, the photochemical thrombosis induction system and a standardized rabbit ischemic stroke model that uses this system have the potential to be used for verifications of biomedical techniques for ischemic stroke at a preclinical stage in parallel with further performance improvements.


2006 ◽  
Vol 154 (1-2) ◽  
pp. 233-238 ◽  
Author(s):  
Vincent A. DiNapoli ◽  
Charles L. Rosen ◽  
Tomoaki Nagamine ◽  
Todd Crocco

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e66393 ◽  
Author(s):  
Fu Jia Liu ◽  
Kai Ying Lim ◽  
Prameet Kaur ◽  
Sugunavathi Sepramaniam ◽  
Arunmozhiarasi Armugam ◽  
...  

2018 ◽  
Vol 26 (10) ◽  
pp. 2357-2365 ◽  
Author(s):  
Bettina Buchthal ◽  
Ursula Weiss ◽  
Hilmar Bading

Stroke ◽  
1992 ◽  
Vol 23 (8) ◽  
pp. 1167-1173 ◽  
Author(s):  
K Overgaard ◽  
T Sereghy ◽  
G Boysen ◽  
H Pedersen ◽  
N H Diemer

1994 ◽  
Vol 14 (3) ◽  
pp. 472-477 ◽  
Author(s):  
Karsten Overgaard ◽  
Tomas Sereghy ◽  
Hans Pedersen ◽  
Gudrun Boysen

The effect of delayed thrombolysis with recombinant tissue plasminogen activator was tested in an embolic stroke model. The carotid territory was embolized in 103 rats with fibrin-rich clots formed and washed in polyethylene tubes. Hemispheric cerebral blood flow before and after embolization was measured by the intra arterial 133Xe injection method. At five delay times, 15–240 min after embolization, 69 animals were treated with tissue plasminogen activator, 20 mg/kg, and 34 animals with saline. Carotid angiography displayed the grade of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after 2 days, evaluated neuropathologically, and infarct volume measured. Cerebral blood flow was reduced by 56–71% after embolization. Reperfusion induced by thrombolytic therapy was demonstrated by comparing the posttreatment angiography of the pooled five treatment groups to control animals. Thrombolytic therapy significantly reduced the infarct volume and improved the prekill clinical score by up to 2 h of treatment delay, and treatment might have been beneficial even after 4 h delay. Prolonging the delay of treatment increased the infarct volume ( p < 0.001, Jonckheere–Terpstra test). Only a few hemorrhagic complications were observed. Thus, thrombolytic therapy in embolic stroke induced recanalization. The effect on clinical outcome and infarct volume was dependent on delay time.


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