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Roles of autophagy and endoplasmic reticulum stress in intracerebral hemorrhage-induced secondary brain injury in rats.

Authors: Duan, Xiao-Chun  Wang, Wei  Feng, Dong-Xia  Yin, Jia  Zuo, Gang  Chen, Dong-Dong  Chen, Zhou-Qing  Li, Hai-Ying  Wang, Zhong  Chen, Gang 
Citation: Duan XC, etal., CNS Neurosci Ther. 2017 Jul;23(7):554-566. doi: 10.1111/cns.12703. Epub 2017 May 19.
Pubmed: (View Article at PubMed) PMID:28544790
DOI: Full-text: DOI:10.1111/cns.12703


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.

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RGD Object Information
RGD ID: 13782167
Created: 2018-08-24
Species: All species
Last Modified: 2018-08-24
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.