Inhibitory effects of curcuminoids on dexamethasone-induced muscle atrophy in differentiation of C2C12 cells
2021
Sani, Asron | Hasegawa, Kazuya | Yamaguchi, Yuya | Panichayupakaranant, Pharkphoom | Pengjam, Yutthana
Sarcopenia is a disease of progressive loss of muscle mass due to the imbalance of protein synthesis and proteolysis, and tends to emerge with ageing. Currently its treatment consists of non-drug therapies and drug therapies, but some medications can have various side effects. Therefore, it is important to search for effective herbal medicines that can modulate muscle mass. In this study, we investigated the inhibition effects of Cu, De, Bis, CRE, CRE-SD, CRE-Bin, and CRE-Ter on dexamethasone-induced muscle atrophy in differentiation of C2C12 cells. C2C12 cells were cultured and treated with various concentrations of curcuminoids including, Cu, De, Bis, CRE, CRE-SD, CRE-Bin, and CRE-Ter. The inhibitory effects were studied using various methods, including MTT and LDH assays for cell viability and cell cytotoxicity, RT-qPCR for gene expression analysis, and Western blots for protein analysis. In this study, dexamethasone-treated C2C12 myotubes (Dex) are the positive drug control and used as in vitro models of muscle atrophy. The results revealed that treating differentiated C2C12 cells with Cu, CRE, CRE-Bin, and CRE-Ter reduced Atrogin-1 and MuRF-1 expression, whereas CRE-SD reduced only MuRF-1 expression. The Western blot analysis results show that Cu, CRE, CRE-Bin, CRE-Ter, and CRE-SD upregulated the phosphorylation level of Akt, which is an important protein in the mTOR signaling pathway. Our results show that Cu, CRE, CRE-Bin, CRE-SD, and CRE-Ter tend to inhibit muscle atrophy by decreasing expression of Atrogin-1 and MuRF-1 inhibiting protein degradation, and to upregulate Phospho-Akt to stimulate protein synthesis. These results provide corroborating evidence of therapeutic potential to treat sarcopenia patients.
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