Preventive Effects of Schisandrin A, A Bioactive Component of Schisandra chinensis, on Dexamethasone-Induced Muscle Atrophy.

Myeonghoon Yeon,Hee-Sook Jun,Hojung Choi

doi:10.3390/nu12051255

Myeonghoon Yeon, Hee-Sook Jun + Show 1 more

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https://doi.org/10.3390/nu12051255

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Journal: Nutrients	Publication Date: Apr 28, 2020
Citations: 19	License type: CC BY 4.0

Affiliation: Gachon University, Gachon University Gil Hospital

Abstract

Muscle wasting is caused by various factors, such as aging, cancer, diabetes, and chronic kidney disease, and significantly decreases the quality of life. However, therapeutic interventions for muscle atrophy have not yet been well-developed. In this study, we investigated the effects of schisandrin A (SNA), a component extracted from the fruits of Schisandra chinensis, on dexamethasone (DEX)-induced muscle atrophy in mice and studied the underlying mechanisms. DEX+SNA-treated mice had significantly increased grip strength, muscle weight, and muscle fiber size compared with DEX+vehicle-treated mice. In addition, SNA treatment significantly reduced the expression of muscle degradation factors such as myostatin, MAFbx (atrogin1), and muscle RING-finger protein-1 (MuRF1) and enhanced the expression of myosin heavy chain (MyHC) compared to the vehicle. In vitro studies using differentiated C2C12 myotubes also showed that SNA treatment decreased the expression of muscle degradation factors induced by dexamethasone and increased protein synthesis and expression of MyHCs by regulation of Akt/FoxO and Akt/70S6K pathways, respectively. These results suggest that SNA reduces protein degradation and increases protein synthesis in the muscle, contributing to the amelioration of dexamethasone-induced muscle atrophy and may be a potential candidate for the prevention and treatment of muscle atrophy.

Highlights

Skeletal muscle atrophy is caused by several factors including genetic factors, various diseases, disuse, and aging [1]
The maintenance of muscle mass depends on the balance between protein degradation and synthesis, and both these processes are sensitive to factors such as hormonal balance, nutritional status, physical activity/exercise, injury, and disease [3]
We found that schisandrin A (SNA) treatment increased the muscle mass and grip strength in DEX-induced muscle atrophy in mice by blocking protein degradation and stimulating protein synthesis

Summary

Introduction

Skeletal muscle atrophy is caused by several factors including genetic factors, various diseases, disuse, and aging [1]. As the lifespan of humans increases with the development of medicine, age-associated skeletal muscle atrophies are becoming a global social problem due to deterioration of the quality of life [2]. Many studies are being conducted to develop therapeutic drugs for the treatment of muscle atrophy. The maintenance of muscle mass depends on the balance between protein degradation and synthesis, and both these processes are sensitive to factors such as hormonal balance, nutritional status, physical activity/exercise, injury, and disease [3]. Muscle protein degradation occurs through the ubiquitin-proteasome-dependent pathway, caspase system pathway, and autophagy pathway [4]

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