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Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment

Skeletal muscle satellite cells are heavily involved in the regeneration of skeletal muscle in response to the aging-related deterioration of the skeletal muscle mass, strength, and regenerative capacity, termed as sarcopenia. This study focused on the effect of tocotrienol rich fraction (TRF) on re...

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Autores principales: Lim, Jing Jye, Wan Ngah, Wan Zurinah, Mouly, Vincent, Abdul Karim, Norwahidah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856141/
https://www.ncbi.nlm.nih.gov/pubmed/24349615
http://dx.doi.org/10.1155/2013/978101
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author Lim, Jing Jye
Wan Ngah, Wan Zurinah
Mouly, Vincent
Abdul Karim, Norwahidah
author_facet Lim, Jing Jye
Wan Ngah, Wan Zurinah
Mouly, Vincent
Abdul Karim, Norwahidah
author_sort Lim, Jing Jye
collection PubMed
description Skeletal muscle satellite cells are heavily involved in the regeneration of skeletal muscle in response to the aging-related deterioration of the skeletal muscle mass, strength, and regenerative capacity, termed as sarcopenia. This study focused on the effect of tocotrienol rich fraction (TRF) on regenerative capacity of myoblasts in stress-induced premature senescence (SIPS). The myoblasts was grouped as young control, SIPS-induced, TRF control, TRF pretreatment, and TRF posttreatment. Optimum dose of TRF, morphological observation, activity of senescence-associated β-galactosidase (SA-β-galactosidase), and cell proliferation were determined. 50 μg/mL TRF treatment exhibited the highest cell proliferation capacity. SIPS-induced myoblasts exhibit large flattened cells and prominent intermediate filaments (senescent-like morphology). The activity of SA-β-galactosidase was significantly increased, but the proliferation capacity was significantly reduced as compared to young control. The activity of SA-β-galactosidase was significantly reduced and cell proliferation was significantly increased in the posttreatment group whereas there was no significant difference in SA-β-galactosidase activity and proliferation capacity of pretreatment group as compared to SIPS-induced myoblasts. Based on the data, we hypothesized that TRF may reverse the myoblasts aging through replenishing the regenerative capacity of the cells. However, further investigation on the mechanism of TRF in reversing the myoblast aging is needed.
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spelling pubmed-38561412013-12-16 Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment Lim, Jing Jye Wan Ngah, Wan Zurinah Mouly, Vincent Abdul Karim, Norwahidah Oxid Med Cell Longev Research Article Skeletal muscle satellite cells are heavily involved in the regeneration of skeletal muscle in response to the aging-related deterioration of the skeletal muscle mass, strength, and regenerative capacity, termed as sarcopenia. This study focused on the effect of tocotrienol rich fraction (TRF) on regenerative capacity of myoblasts in stress-induced premature senescence (SIPS). The myoblasts was grouped as young control, SIPS-induced, TRF control, TRF pretreatment, and TRF posttreatment. Optimum dose of TRF, morphological observation, activity of senescence-associated β-galactosidase (SA-β-galactosidase), and cell proliferation were determined. 50 μg/mL TRF treatment exhibited the highest cell proliferation capacity. SIPS-induced myoblasts exhibit large flattened cells and prominent intermediate filaments (senescent-like morphology). The activity of SA-β-galactosidase was significantly increased, but the proliferation capacity was significantly reduced as compared to young control. The activity of SA-β-galactosidase was significantly reduced and cell proliferation was significantly increased in the posttreatment group whereas there was no significant difference in SA-β-galactosidase activity and proliferation capacity of pretreatment group as compared to SIPS-induced myoblasts. Based on the data, we hypothesized that TRF may reverse the myoblasts aging through replenishing the regenerative capacity of the cells. However, further investigation on the mechanism of TRF in reversing the myoblast aging is needed. Hindawi Publishing Corporation 2013 2013-11-20 /pmc/articles/PMC3856141/ /pubmed/24349615 http://dx.doi.org/10.1155/2013/978101 Text en Copyright © 2013 Jing Jye Lim et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Lim, Jing Jye
Wan Ngah, Wan Zurinah
Mouly, Vincent
Abdul Karim, Norwahidah
Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title_full Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title_fullStr Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title_full_unstemmed Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title_short Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
title_sort reversal of myoblast aging by tocotrienol rich fraction posttreatment
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856141/
https://www.ncbi.nlm.nih.gov/pubmed/24349615
http://dx.doi.org/10.1155/2013/978101
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