%0 Journal Article
%T Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment
%A Jing Jye Lim
%A Wan Zurinah Wan Ngah
%A Vincent Mouly
%A Norwahidah Abdul Karim
%J Oxidative Medicine and Cellular Longevity
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/978101
%X 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 ¦Â-galactosidase (SA-¦Â-galactosidase), and cell proliferation were determined. 50£¿¦Ìg/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-¦Â-galactosidase was significantly increased, but the proliferation capacity was significantly reduced as compared to young control. The activity of SA-¦Â-galactosidase was significantly reduced and cell proliferation was significantly increased in the posttreatment group whereas there was no significant difference in SA-¦Â-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. 1. Introduction Skeletal muscle composes 45 to 55% of the total body mass and can be considered as the largest organ in the body [1]. It is a postmitotic tissue which mainly is composed of multinucleated myofibres [2]. The regeneration capability of skeletal muscle to adapt with the normal physiology growth and to compensate with the wear and tear of skeletal muscle due to injury or disease is highly dependent on a population of quiescent progenitors, known as satellite cells [3, 4]. These quiescent mononucleated cells are sequestered between the basal lamina and sarcolemma of myofibres, as originally described by Mauro [5]. These satellite cells were known as myoblasts once they were isolated from muscle biopsies and proliferate in culture [6]. The quiescent satellite cells were activated in response to damage or exercise and proliferated as myoblasts, which further differentiated and fused to repair or form the muscle fibers [7]. Unfortunately, neither skeletal muscle nor the satellite cells could avoid the fate of various modifications during
%U http://www.hindawi.com/journals/omcl/2013/978101/