scholarly journals Long Noncoding RNA H19 Overexpression Protects against Hypoxic-Ischemic Brain Damage by Inhibiting miR-107 and Up-Regulating Vascular Endothelial Growth Factor

2021 ◽  
Vol 191 (3) ◽  
pp. 503-514
Author(s):  
Hua Fang ◽  
Hua-Feng Li ◽  
Qin Pan ◽  
Miao Yang ◽  
Fang-Xiang Zhang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Brain Damage ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Vascular Endothelial ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Endothelial Growth Factor

scholarly journals Reduction of Ischemic Damage by Application of Vascular Endothelial Growth Factor in Rat Brain after Transient Ischemia

1998 ◽  
Vol 18 (8) ◽  
pp. 887-895 ◽  
Author(s):  
Takeshi Hayashi ◽  
Koji Abe ◽  
Yasuto Itoyama
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Rat Brain ◽  
Evans Blue ◽  
Infarct Volume ◽  
Vascular Endothelial ◽  
Transient Ischemia ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a secreted polypeptide and plays a pivotal role in angiogenesis in vivo. However, it also increases vascular permeability, and might exacerbate ischemic brain edema. The effect of this factor on the brain after transient ischemia was investigated in terms of infarct volume and edema formation, as well as cellular injury. After 90 minutes of transient middle cerebral artery occlusion, VEGF (1.0 ng/μL, 9 μL) was topically applied on the surface of the reperfused rat brain. A significant reduction of infarct volume was found in animals with VEGF application ( P < 0.001) at 24 hours of reperfusion as compared with cases with vehicle treatment. Brain edema was significantly reduced in VEGF-treated animals ( P = 0.01), and furthermore, extravasation of Evans blue was also decreased in those animals ( P < 0.01). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling and immunohistochemical analysis for 70-kDa heat shock protein showed an amelioration of the stainings at 24 and 48 hours after reperfusion with VEGF treatment, which indicated reduction of neuronal damage. These results indicate that treatment with topical VEGF application significantly reduces ischemic brain damage, such as infarct volume, edema formation, and extravasation of Evans blue, and that the reductions were associated with that of neuronal injury.

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