The Effects of Tetra hydrobiopterin on Intracerebral Hemorrhage-Induced Brain Injury in Mice

被引:2
|
作者
Tsuchiyama, Reiko [1 ]
Sozen, Takumi [1 ]
Titova, Elena [2 ]
Zhang, John H. [1 ]
Tang, Jiping [1 ]
机构
[1] Loma Linda Univ, Med Ctr, Dept Physiol & Pharmacol, 11041 Campus St,Risley Hall Room 133, Loma Linda, CA 92354 USA
[2] Loma Linda Univ, Dept Radiat Med, Loma Linda, CA 92350 USA
来源
BRAIN EDEMA XIV | 2010年 / 106卷
关键词
Tetrahydrobiopterin(BH4); ICH; mice; brain edema; NITRIC-OXIDE SYNTHASE; ISCHEMIA-REPERFUSION INJURY; ENDOTHELIAL DYSFUNCTION; SUPEROXIDE GENERATION; TETRAHYDROBIOPTERIN; RATS; INVOLVEMENT;
D O I
10.1007/978-3-211-98811-4_28
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase (NOS) and is presently used clinically to treat forms of phenylketonuria. BH4 has been reported to restrain superoxide generation of NOS and chemically reduce superoxide. However, there has been no report concerning the effects of BH4 in intracerebral hemorrhage (ICH). In the present study, we investigated the neuroprotective effect of BH4 against ICH-induced brain injury in a mouse model. A total of 26 male CD 1 mice (31-39 g) were divided into sham, ICH-vehicle, and ICH-treated with BH4 groups (n = 8 in each group). ICH was induced by collagenase injection into the right basal ganglia. BH4 (20 mg/kg) was administrated intraperitoneally at 1 h after ICH. The effect of BH4 was measured by neurological score and brain water content at 24 h after ICH. Our data demonstrates that ICH caused significant neurological deficit that is associated with brain edema. Treatment with BH4 did not reduce brain edema and neurological deficits at 24 h after ICH in mice. Further study is required to investigate the long-term effect of BH4 in ICH-induced brain injury.
引用
收藏
页码:155 / +
页数:2
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