PMID- 28048972
OWN - NLM
STAT- MEDLINE
DCOM- 20170807
LR  - 20191210
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1659
DP  - 2017 Mar 15
TI  - Astaxanthin improves cognitive performance in mice following mild traumatic brain 
      injury.
PG  - 88-95
LID - S0006-8993(16)30860-5 [pii]
LID - 10.1016/j.brainres.2016.12.031 [doi]
AB  - BACKGROUND: Traumatic brain injury (TBI) produces lasting neurological deficits 
      that plague patients and physicians. To date, there is no effective method to 
      combat the source of this problem. Here, we utilized a mild, closed head TBI 
      model to determine the modulatory effects of a natural dietary compound, 
      astaxanthin (AST). AST is centrally active following oral administration and is 
      neuroprotective in experimental brain ischemia/stroke and subarachnoid hemorrhage 
      (SAH) models. We examined the effects of oral AST on the long-term neurological 
      functional recovery and histological outcomes following moderate TBI in a mice 
      model. METHODS: Male adult ICR mice were divided into 3 groups: (1) Sham+olive 
      oil vehicle treated, (2) TBI+olive oil vehicle treated, and (3) TBI+AST. The 
      olive oil vehicle or AST were administered via oral gavage at scheduled time 
      points. Closed head brain injury was applied using M.A. Flierl weight-drop 
      method. NSS, Rotarod, ORT, and Y-maze were performed to test the behavioral or 
      neurological outcome. The brain sections from the mice were stained with H&E and 
      cresyl-violet to test the injured lesion volume and neuronal loss. Western blot 
      analysis was performed to investigate the mechanisms of neuronal cell survival 
      and neurological function improvement. RESULTS: AST administration improved the 
      sensorimotor performance on the Neurological Severity Score (NSS) and rotarod 
      test and enhanced cognitive function recovery in the object recognition test 
      (ORT) and Y-maze test. Moreover, AST treatment reduced the lesion size and 
      neuronal loss in the cortex compared with the vehicle-treated TBI group. AST also 
      restored the levels of brain-derived neurotropic factor (BDNF), growth-associated 
      protein-43 (GAP-43), synapsin, and synaptophysin (SYP) in the cerebral cortex, 
      which indicates the promotion of neuronal survival and plasticity. CONCLUSION: To 
      the best of our knowledge, this is the first study to demonstrate the protective 
      role and the underlining mechanism of AST in TBI. Based on these neuroprotective 
      actions and considering its longstanding clinical use, AST should be considered 
      for the clinical treatment of TBI.
CI  - Copyright A(c) 2017 Elsevier B.V. All rights reserved.
FAU - Ji, Xinran
AU  - Ji X
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
FAU - Peng, Dayong
AU  - Peng D
AD  - Department of Orthopedics, Shandong Qianfoshan Hospital, Shandong University, 
      Jing Shi Road, Jinan, Shandong 250014, China.
FAU - Zhang, Yiling
AU  - Zhang Y
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
FAU - Zhang, Jun
AU  - Zhang J
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
FAU - Wang, Yuning
AU  - Wang Y
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
FAU - Gao, Yuan
AU  - Gao Y
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
FAU - Lu, Ning
AU  - Lu N
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China. 
      Electronic address: luning301@126.com.
FAU - Tang, Peifu
AU  - Tang P
AD  - The Department of Orthopaedic Surgery, Chinese People's Liberation Army General 
      Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China. 
      Electronic address: tangpeifu301@126.com.
LA  - eng
PT  - Journal Article
DEP - 20161231
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Nootropic Agents)
RN  - 0 (Xanthophylls)
RN  - 8XPW32PR7I (astaxanthine)
SB  - IM
MH  - Animals
MH  - Brain Concussion/*drug therapy/metabolism/pathology/*psychology
MH  - Cerebral Cortex/drug effects/metabolism/pathology
MH  - Cognition/*drug effects
MH  - Disease Models, Animal
MH  - Dose-Response Relationship, Drug
MH  - Drug Evaluation, Preclinical
MH  - Male
MH  - Maze Learning/drug effects
MH  - Mice, Inbred ICR
MH  - Neurons/drug effects/metabolism/pathology
MH  - Neuroprotective Agents/*pharmacology
MH  - Nootropic Agents/*pharmacology
MH  - Recognition, Psychology/drug effects
MH  - Rotarod Performance Test
MH  - Severity of Illness Index
MH  - Spatial Memory/drug effects
MH  - Xanthophylls/pharmacology
OTO - NOTNLM
OT  - Astaxanthin
OT  - Growth-associated protein
OT  - NSS
OT  - Object recognition test
OT  - Rotarod test
OT  - Synaptic protein
OT  - Traumatic brain injury
OT  - Y-maze
EDAT- 2017/01/04 06:00
MHDA- 2017/08/08 06:00
CRDT- 2017/01/04 06:00
PHST- 2016/09/14 00:00 [received]
PHST- 2016/12/30 00:00 [accepted]
PHST- 2017/01/04 06:00 [pubmed]
PHST- 2017/08/08 06:00 [medline]
PHST- 2017/01/04 06:00 [entrez]
AID - S0006-8993(16)30860-5 [pii]
AID - 10.1016/j.brainres.2016.12.031 [doi]
PST - ppublish
SO  - Brain Res. 2017 Mar 15;1659:88-95. doi: 10.1016/j.brainres.2016.12.031. Epub 2016 
      Dec 31.