Gastrodia elata blume and an active component, p-hydroxybenzyl alcohol reduce focal ischemic brain injury through antioxidant related gene expressions

被引:93
作者
Yu, SJ
Kim, JR
Lee, CK
Han, JE
Lee, JH
Kim, HS
Hong, JH
Kang, SG [1 ]
机构
[1] Inje Univ, Inst Basic Sci, Sch Biotechnol & Biomed Sci, Gimhae 621749, South Korea
[2] Inje Univ, Inst Ind Med, Pusan 614735, South Korea
[3] Inje Univ, Dept Food Sci & Engn, Gimhae 621749, South Korea
[4] Okayama Univ, Fac Pharmaceut Sci, Okayama 7008530, Japan
关键词
1-Cys peroxiredoxin; Gastrodia elata blume; ischemia; p-hydroxybenzyl alcohol; protein disulfide isomerase;
D O I
10.1248/bpb.28.1016
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Ischaemic stroke is a leading cause of death and long-lasting disability. Gastrodia elata blume (GEB) is a Chinese herb that is widely used to treat convulsive disorders, such as epilepsy, and p-hydroxybenzyl alcohol (HBA) is the active ingredient in GEB. The present study was conducted to evaluate the effects of GEB and HBA on the brain damage and transcriptional levels of Protein disulfide isomerase (PDI) and 1-Cys peroxiredoxin (1-Cys Prx) genes known to play a role in antioxidant systems after transient focal ischemia in the rat brain. Focal ischemia was induced in rats by middle cerebral artery occlusion (MCAO). All animals underwent ischemia for I h, followed by 24 h of reperfusion. Coronal brain slices were stained with 2,3,5-triphenyltetrazolium chloride or total RNA was extracted for the analysis of gene expression. Histopathologic analysis revealed a significant (p < 0.05) decrease in infarct size in the ipsilateral brain with GEB extracts or HBA. Moreover, the levels of PDI and 1-Cys Prx transcription were significantly increased in the GEB extract- or HBA-treated group compared with the untreated group (p < 0.05). This study therefore indicated that GEB and HBA provide neuroprotection by preventing brain damage through the increased expression of genes encoding antioxidant proteins after transient focal cerebral ischemia and may be effective as neuroprotective agents at the cellular and molecular levels in the brain.
引用
收藏
页码:1016 / 1020
页数:5
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