Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment - Sorbonne Université
Article Dans Une Revue Oxidative Medicine and Cellular Longevity Année : 2013

Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment

Résumé

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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Dates et versions

hal-01596040 , version 1 (27-09-2017)

Identifiants

Citer

Jing Jye Lim, Wan Zurinah Wan Ngah, Vincent Mouly, Norwahidah Abdul Karim. Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment. Oxidative Medicine and Cellular Longevity, 2013, 2013, pp.978101. ⟨10.1155/2013/978101⟩. ⟨hal-01596040⟩
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