scholarly journals Dehydroascorbic Acid Attenuates Ischemic Brain Edema and Neurotoxicity in Cerebral Ischemia: An in vivo Study

2015 ◽  
Vol 24 (1) ◽  
pp. 41-54 ◽  
Author(s):  
Juhyun Song ◽  
Joohyun Park ◽  
Jae Hwan Kim ◽  
Ja Yong Choi ◽  
Jae Young Kim ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Edema ◽  
Dehydroascorbic Acid ◽  
In Vivo Study ◽  
Ischemic Brain ◽  
Ischemic Brain Edema

Time-lag combination therapy for cerebral ischemia using the FNK protein transduction technology and an immunosuppressant, I: In vivo study

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S57-S57
Author(s):  
Ken-ichiro Kasura ◽  
Megumi Watanabe ◽  
Kumiko Takahashi ◽  
Genki Mizukoshi ◽  
Seiji Ohkubo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Combination Therapy ◽  
Time Lag ◽  
In Vivo Study ◽  
Protein Transduction

scholarly journals Poldip2 controls leukocyte infiltration into the ischemic brain by regulating focal adhesion kinase-mediated VCAM-1 induction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lori N. Eidson ◽  
Qingzeng Gao ◽  
Hongyan Qu ◽  
Daniel S. Kikuchi ◽  
Ana Carolina P. Campos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebral Ischemia ◽  
Focal Adhesion Kinase ◽  
Adhesion Molecules ◽  
Focal Adhesion ◽  
Vascular Inflammation ◽  
Leukocyte Recruitment ◽  
Ischemic Brain ◽  
Inflammatory Monocytes

AbstractStroke is a multiphasic process involving a direct ischemic brain injury which is then exacerbated by the influx of immune cells into the brain tissue. Activation of brain endothelial cells leads to the expression of adhesion molecules such vascular cell adhesion molecule 1 (VCAM-1) on endothelial cells, further increasing leukocyte recruitment. Polymerase δ-interacting protein 2 (Poldip2) promotes brain vascular inflammation and leukocyte recruitment via unknown mechanisms. This study aimed to define the role of Poldip2 in mediating vascular inflammation and leukocyte recruitment following cerebral ischemia. Cerebral ischemia was induced in Poldip2+/+ and Poldip2+/− mice and brains were isolated and processed for flow cytometry or RT-PCR. Cultured rat brain microvascular endothelial cells were used to investigate the effect of Poldip2 depletion on focal adhesion kinase (FAK)-mediated VCAM-1 induction. Poldip2 depletion in vivo attenuated the infiltration of myeloid cells, inflammatory monocytes/macrophages and decreased the induction of adhesion molecules. Focusing on VCAM-1, we demonstrated mechanistically that FAK activation was a critical intermediary in Poldip2-mediated VCAM-1 induction. In conclusion, Poldip2 is an important mediator of endothelial dysfunction and leukocyte recruitment. Thus, Poldip2 could be a therapeutic target to improve morbidity following ischemic stroke.

scholarly journals Proton NMR relaxation times in ischemic brain edema.

Stroke ◽  
1986 ◽  
Vol 17 (6) ◽  
pp. 1149-1152 ◽  
Author(s):  
Y Horikawa ◽  
S Naruse ◽  
C Tanaka ◽  
K Hirakawa ◽  
H Nishikawa
Keyword(s):  
Brain Edema ◽  
Relaxation Times ◽  
Proton Nmr ◽  
Nmr Relaxation ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Nmr Relaxation Times

scholarly journals Experimental brain infarcts in cats. II. Ischemic brain edema.

Stroke ◽  
1980 ◽  
Vol 11 (6) ◽  
pp. 593-601 ◽  
Author(s):  
F J Schuier ◽  
K A Hossmann
Keyword(s):  
Brain Edema ◽  
Ischemic Brain ◽  
Brain Infarcts ◽  
Ischemic Brain Edema

scholarly journals Transport of sodium from blood to brain in ischemic brain edema.

Stroke ◽  
1987 ◽  
Vol 18 (1) ◽  
pp. 150-157 ◽  
Author(s):  
W D Lo ◽  
A L Betz ◽  
G P Schielke ◽  
J T Hoff
Keyword(s):  
Brain Edema ◽  
Ischemic Brain ◽  
Ischemic Brain Edema

The function of aquaporin4 in ischemic brain edema

2014 ◽  
Vol 127 ◽  
pp. 5-9 ◽  
Author(s):  
Wen-Wen Wang ◽  
Cheng-long Xie ◽  
Li-Li Zhou ◽  
Guo-Sheng Wang
Keyword(s):  
Brain Edema ◽  
Ischemic Brain ◽  
Ischemic Brain Edema
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