Zinc oxide nanoparticles promoting the formation of myogenic differentiation into myotubes in mouse myoblast C2C12 cells

被引:17
|
作者
Ramalingam, Vaikundamoorthy [1 ]
Hwang, Inho [1 ]
机构
[1] Chonbuk Natl Univ, Dept Anim Sci, Jeonju 561756, South Korea
关键词
ZnOnanoparticles; Characterization; Myoblasts; Myogenic differentiation; Molecular mechanism; SKELETAL-MUSCLE DIFFERENTIATION; HUMAN HEALTH; ZNO NANOPARTICLES; NANOSTRUCTURES; ACTIVATION; APOPTOSIS; CASPASE-3; PI3K/AKT; ENHANCE; GOLD;
D O I
10.1016/j.jiec.2019.12.004
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
In the present study, we investigated the effect of monodispersed zinc oxide (ZnO) nanoparticles on the proliferation, myogenic differentiation and regulation of associated myogenic marker genes. The asprepared ZnO nanoparticles had the hexagonal wurtzite structure with maximum absorption at 355 nm and the band gap energy was found to be 3.21 eV. The electron microscopy analysis showed that the ZnO nanoparticles are spherical in shape with an average size range between 10 to 15 nm. The XRD analysis confirmed the hexagonal structure of ZnO nanoparticles and the Raman spectroscopic analysis showed the vibrations of the zinc lattice and oxygen vibration of ZnO nanoparticles. The effect of ZnO nanoparticles on myogenic differentiation was analyzed using C2C12 cells and the results showed the nanoparticles supported the proliferation with negotiable cytotoxic activity. Moreover, the ZnO nanoparticles were significantly enhanced the myoblasts into myotube formation through upregulating the myogenic markers such as myosin heavy chain, MyoD, MyoG genes. The further analysis demonstrated that the ZnO nanoparticles regulates the non-apoptotic effect of caspases and calpain family proteins in respond to the enhancement of myogenic differentiation. Together, the ZnO nanoparticles provide an additional evidence for the role of nanomaterials in skeletal muscle repair and tissue regeneration engineering. (C) 2019 The Korean Society of Industrial and Engineering Chemistry. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:315 / 322
页数:8
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