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Brain Res. 2017 Mar 15;1659:88-95. doi: 10.1016/j.brainres.2016.12.031. Epub 2016 Dec 31.

Astaxanthin improves cognitive performance in mice following mild traumatic brain injury.

Author information

1
The Department of Orthopaedic Surgery, Chinese People's Liberation Army General Hospital (301 Hospital), 28 Fuxing Road, Wukesong, Beijing 100000, China.
2
Department of Orthopedics, Shandong Qianfoshan Hospital, Shandong University, Jing Shi Road, Jinan, Shandong 250014, China.
3
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.
4
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.

Abstract

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.

KEYWORDS:

Astaxanthin; Growth-associated protein; NSS; Object recognition test; Rotarod test; Synaptic protein; Traumatic brain injury; Y-maze

PMID:
28048972
DOI:
10.1016/j.brainres.2016.12.031
[Indexed for MEDLINE]

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