|
KMID : 1149220200280010029
|
|
Korean Journal of Oriental Medical Prescription
2020 Volume.28 No. 1 p.29 ~ p.39
|
|
|
Effects of glucoraphanin in dexamethasone-induced skeletal muscle atrophy in vitro model
|
|
Jeon Sang-Kyu
Kim Ok-Hyeon
Park Su-Mi
Lee Ju-Hee
Park Sun-Dong
|
|
|
Abstract
|
|
|
Objectives : Glucoraphanin is one of the well-known natural glucosinolates found in cruciferous plants. In the present study, we investigated the effects and molecular mechanism of glucoraphanin in dexamethasone-induced skeletal muscle atrophy in vitro model.
Methods : The cytotoxic effects of glucoraphanin on C2C12 myoblasts or myotubes were evaluated by MTT assay. The glucoraphanin was evaluated effects in dexamethasone-induced skeletal muscle atrophy in C2C12 myotubes using a real-time PCR, western blots analysis, and immunofluorescence staining of myosin heavy chain.
Result : Glucoraphanin had no cytotoxicity on both C2C12 myoblasts or myotubes. Dexamethasone markedly induced muscle atrophy by up-regulating muscle-specific ubiquitin E3 ligase markers, atrogin-1 and MuRF1, and down-regulating MyoD, a myogenic regulatory factor whereas co-treatment of glucoraphanin and dexamethasone dose-dependently inhibited it. Furthermore, decreased expressions of p-Akt, p-FOXO1, and p-FOXO3a induced by dexamethasone were reversed by co-treatment with glucoraphanin and dexamethasone. In addition, dexamethasone obviously reduced myotube diameters, while co-treatment of glucoraphanin and dexamethasone increased those to a similar level as control.
Conclusions : These results show that glucoraphanin suppresses dexamethasone-induced muscle atrophy in C2C12 myotubes through activation of Akt/FOXO signaling pathway.
|
|
|
KEYWORD
|
|
|
Glucoraphanin, C2C12, dexamethasone, muscle atrophy, Akt, FOXO
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|