PMID- 26964766
OWN - NLM
STAT- MEDLINE
DCOM- 20171212
LR  - 20180103
IS  - 1872-9754 (Electronic)
IS  - 0197-0186 (Linking)
VI  - 96
DP  - 2016 Jun
TI  - Autophagy regulates intracerebral hemorrhage induced neural damage via apoptosis 
      and NF-kappaB pathway.
PG  - 100-12
LID - S0197-0186(16)30031-6 [pii]
LID - 10.1016/j.neuint.2016.03.004 [doi]
AB  - Autophagy can be a pro-survival or a pro-death mechanism depending on the 
      context. The role of autophagy in intracerebral hemorrhage (ICH) remains elusive. 
      In this study, in vivo and in vitro experiments have been carried out to 
      investigate the role of autophagy after ICH. Collagenase-induced ICH model in 
      mouse was made for in vivo experiments. Primary cortical neurons cultures were 
      exposed to hemin to mimic ICH in vitro. 3-Methyladenine (3-MA) and rapamycin 
      (RAP) were administrated both in vivo and in vitro. We first measured brain water 
      content and cell death after ICH in model. Expression of LC3, p62/SQSTM1 (p62), 
      Beclin1, Caspase3 and Bcl-2, which have been found related to autophagy and 
      apoptosis, were assessed both in vivo and in vitro. Furthermore, NF-kappaB was 
      detected to explore the potential mechanisms. We found brain edema in ICH model 
      in mouse and the number of Propidium Iodide (PI)-positive cells both in vivo and 
      in vitro were decreased by 3-MA pretreated. Simultaneously, both in vivo and 
      in vitro, 3-MA significantly decreased the expression of LC3-II and Beclin-1, and 
      maintained p62 at high level after ICH. Furthermore, pretreatment with 3-MA 
      downregulated the level of cleaved caspase-3 but upregulated the Bcl-2 level. 
      Conversely, RAP pretreatment reversed all these results above. These data 
      indicated that autophagy activation may deprave ICH induced brain injury in ICH 
      model and neuro-damage may be related to regulating of NF-kappaB pathway and thereby 
      promote inflammation and apoptosis, thus might provide novel therapeutic 
      interventions for ICH.
CI  - Copyright (c) 2016 Elsevier Ltd. All rights reserved.
FAU - Shen, Xi
AU  - Shen X
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Ma, Lu
AU  - Ma L
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Dong, Wenwen
AU  - Dong W
AD  - Department of Forensic Pathology, China Medical University School of Forensic 
      Medicine, Shenyang 110122, China.
FAU - Wu, Qiong
AU  - Wu Q
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Gao, Yuan
AU  - Gao Y
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Luo, Chengliang
AU  - Luo C
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Zhang, Mingyang
AU  - Zhang M
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Chen, Xiping
AU  - Chen X
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China.
FAU - Tao, Luyang
AU  - Tao L
AD  - Department of Forensic Science, Medical School of Soochow University, Suzhou 
      215123, China. Electronic address: luyang.tao@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160308
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (NF-kappa B)
RN  - 5142-23-4 (3-methyladenine)
RN  - JAC85A2161 (Adenine)
SB  - IM
MH  - Adenine/analogs & derivatives/pharmacology
MH  - Animals
MH  - Apoptosis/drug effects/*physiology
MH  - Autophagy/drug effects/*physiology
MH  - Cells, Cultured
MH  - Cerebral Hemorrhage/*metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - NF-kappa B/*metabolism
MH  - Neurons/drug effects/*metabolism/pathology
MH  - Signal Transduction/drug effects/*physiology
OTO - NOTNLM
OT  - Apoptosis
OT  - Autophagy
OT  - Inflammation
OT  - Intracerebral hemorrhage
OT  - Neuron
EDAT- 2016/03/12 06:00
MHDA- 2017/12/13 06:00
CRDT- 2016/03/12 06:00
PHST- 2015/10/25 00:00 [received]
PHST- 2016/02/02 00:00 [revised]
PHST- 2016/03/05 00:00 [accepted]
PHST- 2016/03/12 06:00 [entrez]
PHST- 2016/03/12 06:00 [pubmed]
PHST- 2017/12/13 06:00 [medline]
AID - S0197-0186(16)30031-6 [pii]
AID - 10.1016/j.neuint.2016.03.004 [doi]
PST - ppublish
SO  - Neurochem Int. 2016 Jun;96:100-12. doi: 10.1016/j.neuint.2016.03.004. Epub 2016 
      Mar 8.