Abstract:
OBJECTIVES:This study aimed to evaluate the roles of autophagy and endoplasmic reticulum (ER) stress in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) in rats. METHODS:Autophagy inducer (rapamycin) and inhibitor (3-methyladenine), as well as ER stress activator (tunicamycin, TM) and inhibitor (tauroursodeoxycholic acid, TUDCA), were used. Bafilomycin A1, an inhibitor of autophagosome-lysosome fusion, was used to assess autophagic flux. RESULTS:Autophagy and ER stress were enhanced in the week after ICH. At 6 hours after ICH, autophagy was excessive, while the autophagic flux was damaged at 72 hours and return to be intact at 7 days after ICH. At 6 hours after ICH, ER stress induction by TM could enhance autophagy and lead to caspase 12-mediated apoptosis and neuronal degeneration, which was further aggravated by autophagy induction. At 7 days after ICH, ER stress inhibition by TUDCA still could suppress ICH-induced SBI. And, the effects of TUDCA were enhanced by autophagy induction. CONCLUSIONS:At 6 hours after ICH, excessive autophagy may participate in ER stress-induced brain injury; at 7 days after ICH, autophagy could enhance the protection of ER stress inhibitor possibly via clearing up the cell rubbish generated due to the early-stage damaged autophagic flux.
journal_name
CNS Neurosci Therjournal_title
CNS neuroscience & therapeuticsauthors
Duan XC,Wang W,Feng DX,Yin J,Zuo G,Chen DD,Chen ZQ,Li HY,Wang Z,Chen Gdoi
10.1111/cns.12703subject
Has Abstractpub_date
2017-07-01 00:00:00pages
554-566issue
7eissn
1755-5930issn
1755-5949journal_volume
23pub_type
杂志文章abstract:BACKGROUND:Sunitinib is an inhibitor of the multiple receptor tyrosine kinases (RTKs) for cancer therapy. Some sunitinib analogues could prevent neuronal death induced by various neurotoxins. However, the neuroprotective effects of sunitinib have not been reported. METHODS:Cerebellar granule neurons (CGNs) and SH-SY5Y...
journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
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pub_type: 杂志文章,多中心研究
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章
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更新日期:2015-08-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章
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更新日期:2010-10-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
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更新日期:2013-09-01 00:00:00
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更新日期:2020-02-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章,评审
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更新日期:2011-04-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章,评审
doi:10.1111/j.1755-5949.2010.00198.x
更新日期:2011-12-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
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更新日期:2018-11-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章
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更新日期:2013-09-01 00:00:00
abstract:BACKGROUND AND PURPOSE:ATP-sensitive potassium (K-ATP) channels couple energy metabolism with electric activity, which play important roles in brain diseases including stroke. However, the impacts of Kir6.1-containing K-ATP channels that mainly expressed on glia in stroke remain unclear. METHODS AND RESULTS:In this st...
journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章
doi:10.1111/cns.12117
更新日期:2013-08-01 00:00:00
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journal_title:CNS neuroscience & therapeutics
pub_type: 杂志文章,多中心研究
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更新日期:2019-02-01 00:00:00