Tocotrienol improves learning and memory deficit of aged rats

Nozomi Kaneai, Kazumi Sumitani, Koji Fukui, Taisuke Koike, Hirokatsu Takatsu, Shiro Urano

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

To define whether tocotrienol (T-3) improves cognitive deficit during aging, effect of T-3 on learning and memory functions of aged rats was assessed. It was found that T-3 markedly counteracts the decline in learning and memory function in aged rats. Quantitative analysis of T-3 content in the rat brain showed that the aged rats fed T-3 mixture-supplemented diet revealed the transport of α- and γ-T-3 to the brain. In contrast, normal young rats fed the same diet did not exhibit brain localization. Furthermore, the T-3 inhibited age-related decreases in the expression of certain blood brain barrier (BBB) proteins, including caludin-5, occludin and junctional adhesion molecule (JAM). It was found that the activation of the cellular proto-oncogene c-Src and extracellular signal-regulated protein kinase (ERK), in the mitogen-activated protein kinase (MAPK) cell signaling pathway for neuronal cell death, was markedly inhibited by T-3. These results may reveal that aging induces partial BBB disruption caused by oxidative stress, thereby enabling the transport of T-3 through the BBB to the central nervous system, whereupon neuronal protection may be mediated by inhibition of c-Src and/or ERK activation, resulting in an improvement in age-related cognitive deficits.

Original languageEnglish
Pages (from-to)114-121
Number of pages8
JournalJournal of Clinical Biochemistry and Nutrition
Volume58
Issue number2
DOIs
Publication statusPublished - 2016 Mar 1

Fingerprint

Tocotrienols
Memory Disorders
Rats
Learning
Data storage equipment
Blood-Brain Barrier
Brain
Nutrition
Junctional Adhesion Molecules
Aging of materials
Chemical activation
src Genes
Diet
Cell signaling
Occludin
Oxidative stress
Extracellular Signal-Regulated MAP Kinases
Neurology
Cell death
Mitogen-Activated Protein Kinases

Keywords

  • Aging
  • BBB
  • c-Src
  • Cognitive deficit
  • Tocotrienol

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Kaneai, N., Sumitani, K., Fukui, K., Koike, T., Takatsu, H., & Urano, S. (2016). Tocotrienol improves learning and memory deficit of aged rats. Journal of Clinical Biochemistry and Nutrition, 58(2), 114-121. https://doi.org/10.3164/jcbn.15-52

Tocotrienol improves learning and memory deficit of aged rats. / Kaneai, Nozomi; Sumitani, Kazumi; Fukui, Koji; Koike, Taisuke; Takatsu, Hirokatsu; Urano, Shiro.

In: Journal of Clinical Biochemistry and Nutrition, Vol. 58, No. 2, 01.03.2016, p. 114-121.

Research output: Contribution to journalArticle

Kaneai, N, Sumitani, K, Fukui, K, Koike, T, Takatsu, H & Urano, S 2016, 'Tocotrienol improves learning and memory deficit of aged rats', Journal of Clinical Biochemistry and Nutrition, vol. 58, no. 2, pp. 114-121. https://doi.org/10.3164/jcbn.15-52
Kaneai, Nozomi ; Sumitani, Kazumi ; Fukui, Koji ; Koike, Taisuke ; Takatsu, Hirokatsu ; Urano, Shiro. / Tocotrienol improves learning and memory deficit of aged rats. In: Journal of Clinical Biochemistry and Nutrition. 2016 ; Vol. 58, No. 2. pp. 114-121.
@article{1e99db585a4f4239a4c189ed91a32ec5,
title = "Tocotrienol improves learning and memory deficit of aged rats",
abstract = "To define whether tocotrienol (T-3) improves cognitive deficit during aging, effect of T-3 on learning and memory functions of aged rats was assessed. It was found that T-3 markedly counteracts the decline in learning and memory function in aged rats. Quantitative analysis of T-3 content in the rat brain showed that the aged rats fed T-3 mixture-supplemented diet revealed the transport of α- and γ-T-3 to the brain. In contrast, normal young rats fed the same diet did not exhibit brain localization. Furthermore, the T-3 inhibited age-related decreases in the expression of certain blood brain barrier (BBB) proteins, including caludin-5, occludin and junctional adhesion molecule (JAM). It was found that the activation of the cellular proto-oncogene c-Src and extracellular signal-regulated protein kinase (ERK), in the mitogen-activated protein kinase (MAPK) cell signaling pathway for neuronal cell death, was markedly inhibited by T-3. These results may reveal that aging induces partial BBB disruption caused by oxidative stress, thereby enabling the transport of T-3 through the BBB to the central nervous system, whereupon neuronal protection may be mediated by inhibition of c-Src and/or ERK activation, resulting in an improvement in age-related cognitive deficits.",
keywords = "Aging, BBB, c-Src, Cognitive deficit, Tocotrienol",
author = "Nozomi Kaneai and Kazumi Sumitani and Koji Fukui and Taisuke Koike and Hirokatsu Takatsu and Shiro Urano",
year = "2016",
month = "3",
day = "1",
doi = "10.3164/jcbn.15-52",
language = "English",
volume = "58",
pages = "114--121",
journal = "Journal of Clinical Biochemistry and Nutrition",
issn = "0912-0009",
publisher = "The Society for Free Radical Research Japan",
number = "2",

}

TY - JOUR

T1 - Tocotrienol improves learning and memory deficit of aged rats

AU - Kaneai, Nozomi

AU - Sumitani, Kazumi

AU - Fukui, Koji

AU - Koike, Taisuke

AU - Takatsu, Hirokatsu

AU - Urano, Shiro

PY - 2016/3/1

Y1 - 2016/3/1

N2 - To define whether tocotrienol (T-3) improves cognitive deficit during aging, effect of T-3 on learning and memory functions of aged rats was assessed. It was found that T-3 markedly counteracts the decline in learning and memory function in aged rats. Quantitative analysis of T-3 content in the rat brain showed that the aged rats fed T-3 mixture-supplemented diet revealed the transport of α- and γ-T-3 to the brain. In contrast, normal young rats fed the same diet did not exhibit brain localization. Furthermore, the T-3 inhibited age-related decreases in the expression of certain blood brain barrier (BBB) proteins, including caludin-5, occludin and junctional adhesion molecule (JAM). It was found that the activation of the cellular proto-oncogene c-Src and extracellular signal-regulated protein kinase (ERK), in the mitogen-activated protein kinase (MAPK) cell signaling pathway for neuronal cell death, was markedly inhibited by T-3. These results may reveal that aging induces partial BBB disruption caused by oxidative stress, thereby enabling the transport of T-3 through the BBB to the central nervous system, whereupon neuronal protection may be mediated by inhibition of c-Src and/or ERK activation, resulting in an improvement in age-related cognitive deficits.

AB - To define whether tocotrienol (T-3) improves cognitive deficit during aging, effect of T-3 on learning and memory functions of aged rats was assessed. It was found that T-3 markedly counteracts the decline in learning and memory function in aged rats. Quantitative analysis of T-3 content in the rat brain showed that the aged rats fed T-3 mixture-supplemented diet revealed the transport of α- and γ-T-3 to the brain. In contrast, normal young rats fed the same diet did not exhibit brain localization. Furthermore, the T-3 inhibited age-related decreases in the expression of certain blood brain barrier (BBB) proteins, including caludin-5, occludin and junctional adhesion molecule (JAM). It was found that the activation of the cellular proto-oncogene c-Src and extracellular signal-regulated protein kinase (ERK), in the mitogen-activated protein kinase (MAPK) cell signaling pathway for neuronal cell death, was markedly inhibited by T-3. These results may reveal that aging induces partial BBB disruption caused by oxidative stress, thereby enabling the transport of T-3 through the BBB to the central nervous system, whereupon neuronal protection may be mediated by inhibition of c-Src and/or ERK activation, resulting in an improvement in age-related cognitive deficits.

KW - Aging

KW - BBB

KW - c-Src

KW - Cognitive deficit

KW - Tocotrienol

UR - http://www.scopus.com/inward/record.url?scp=84959518823&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84959518823&partnerID=8YFLogxK

U2 - 10.3164/jcbn.15-52

DO - 10.3164/jcbn.15-52

M3 - Article

VL - 58

SP - 114

EP - 121

JO - Journal of Clinical Biochemistry and Nutrition

JF - Journal of Clinical Biochemistry and Nutrition

SN - 0912-0009

IS - 2

ER -