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Expression of hypoxia-inducible factor 1 alpha and oligodendrocyte lineage gene-1 in cultured brain slices after oxygen-glucose deprivation
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作者 Hong Cui Weijuan Han +1 位作者 Lijun Yang yanzhong chang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第4期328-337,共10页
Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of g... Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of great significance in premature infants with hypoxic-ischemic brain damage There is little evidence of direct regulatory effects of hypoxia-inducible factor le on oligodendrocyte lineage gene-l. In this study, brain slices of Sprague-Dawley rats were cultured and subjected to oxygen-glucose deprivation. Then, slices were transfected with hypoxia-inducible factor la or oligodendrocyte lineage gene-1. The expression levels of hypoxia-inducible factor la and oligodendrocyte lineage gene-1 were significantly up-regulated in rat brains prior to transfection, as detected by immunohistochemical staining. Eight hours after transfection of slices with hypoxia-inducible factor la, oligodendrocyte lineage gene-1 expression was upregulated, and reached a peak 24 hours after transfection. Oligodendrocyte lineage gene-1 transfection induced no significant differences in hypoxia-inducible factor la levels in rat brain tissues with oxygen-glucose deprivation. These experimental findings indicate that hypoxia-inducible factor la can regulate oligodendrocyte lineage gene-1 expression in hypoxic brain tissue, thus repairing the neural impairment. 展开更多
关键词 neural regeneration brain injury biological factors hypoxia-inducible factor la oligodendrocyte lineage gene-1 oxygen-glucose deprivation brain slice culture immunohistochemistry OLIGODENDROCYTE myelin repair premature delivery rat grants-supported paper photographs-containing paper neuroregeneration
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Sodium glutamate and gamma-aminobutyric acid affect iron metabolism in the rat caudate putamen
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作者 Na Wang Peng Guan +3 位作者 Fei Li Yujian Fu Xianglin Duan yanzhong chang 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第21期1644-1649,共6页
Glutamic acid and gamma-aminobutyric acid (GABA) influence iron content in the substantia nigra and globus pallidus, although the mechanisms of action remain unclear. The present study measured iron content and chan... Glutamic acid and gamma-aminobutyric acid (GABA) influence iron content in the substantia nigra and globus pallidus, although the mechanisms of action remain unclear. The present study measured iron content and changes in divalent metal transporter 1 (DMT1) and hephaestin expression in the substantia nigra and caudate putamen, and explored the effects of GABA and glutamic acid on iron metabolism. Results demonstrated that iron content and DMT1 non iron response element [DMT1 (-IRE)] expression were significantly greater but hephaestin expression was significantly lower in the caudate putamen of the monosodium glutamate group compared with the control group. No significant difference in iron content was detected between the GABA and control groups. DMT1 (-IRE) expression was significantly reduced, but hephaestin expressiori was significantly increased in the GABA group compared with the control group. In addition, there was no significant difference in tyrosine hydroxylase expression between monosodium glutamate and GABA groups and the control group. These results suggested that glutamate affected iron metabolism in the caudate putamen by increasing DMTI(-IRE) and decreasing hephaestin expression. In addition, GABA decreased DMT1 (-IRE) expression in the caudate putamen. 展开更多
关键词 GLUTAMATE gamma-aminobutyric acid tyrosine hydroxylase divalent metal transporter 1 non iron response element HEPHAESTIN
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Expression of yeast silencing information regulator 2 in secondary injury of intracerebral hemorrhage
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作者 Na Hu Ran An yanzhong chang 《Journal of Translational Neuroscience》 2021年第1期29-32,共4页
Objective:to investigate the expression of yeast silencing information regulator 2(Sirt2)in the secondary injury of intracerebral hemorrhage(ICH).Methods:twelve Sprague Dawley(SD)rats were randomly divided into a sham... Objective:to investigate the expression of yeast silencing information regulator 2(Sirt2)in the secondary injury of intracerebral hemorrhage(ICH).Methods:twelve Sprague Dawley(SD)rats were randomly divided into a sham group and an ICH group,with six rats in each group.A rat model of ICH was established by injecting collagenase type IV into the right striatum of the rats.The expression of Sirt2 was measured by Western blot and immunohistochemistry after ICH.Result:the behavioral score of the ICH rats was the lowest at 48 h after the operation;therefore the rats at 48 h after surgery were selected as the model rats.The expression of Sirt2 was significantly higher in the striatal tissue of the ICH rats compared with the sham group(P<0.05).Conclusion:the expression of Sirt2 around hematoma in ICH rats decreases,and Sirt2 is expected to become a new target for ICH treatment. 展开更多
关键词 intracerebral hemorrhage(ICH) secondary injury silencing information regulator 2(Sirt2)
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