Curcuma longa L. Water Extract Improves Dexamethasone-Induced Sarcopenia by Modulating the Muscle-Related Gene and Oxidative Stress in Mice.

Shintae Kim,Kyungmi Kim,Woojin Jun,Jeongjin Park

doi:10.3390/antiox10071000

Shintae Kim, Kyungmi Kim + Show 2 more

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https://doi.org/10.3390/antiox10071000

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Abstract

Dexamethasone (DEX) promotes proteolysis, which causes muscle atrophy. Muscle atrophy is connected to sarcopenia. We evaluated the effect of Curcuma longa L. water extract (CLW) on DEX-induced muscle atrophy. ICR mice were divided into three groups (eight mice per group) to investigate the capability of CLW in inhibiting muscle atrophy. The control group (Ex-CON) was administered distilled water (DW) by gavage and subjected to exercise; the muscle atrophy group (Ex-DEX) was administered DW by gavage, an injection of DEX (1 mg/kg body weight/day) intraperitoneally (IP), and subjected to exercise; and the treatment group (Ex-CLW) was administered CLW (1 g/kg body weight/day) by gavage, DEX IP injection, and subjected to exercise. Following the injection of DEX, the expression levels of myostatin, MuRF-1, and Atrogin-1 were increased. However, these expression levels were decreased in the Ex-CLW group, thereby leading to the conclusion that CLW inhibits muscle atrophy. ROS (that was overproduced by DEX) decreased antioxidant enzyme activity and increased malondialdehyde (MDA) levels, which led to muscle atrophy. When CLW was ingested, the antioxidant enzyme activities increased while the MDA levels decreased. These findings suggest that CLW could serve as a natural product for the prevention of muscle atrophy by modulating muscle atrophy-related genes and increasing antioxidant potential.

Highlights

Muscle atrophy refers to a decrease in muscle mass that is caused by aging, a lack of exercise, or diseases, thereby resulting in a faster rate of protein degradation than the rate of protein synthesis [1]
These findings suggest that Curcuma longa L. water extract (CLW) could serve as a natural product for the prevention of muscle atrophy by modulating muscle atrophy-related genes and increasing antioxidant potential
The decrease observed in the Ex-CLW group was similar to that in the Ex-DEX group

Summary

Introduction

Muscle atrophy refers to a decrease in muscle mass that is caused by aging, a lack of exercise, or diseases, thereby resulting in a faster rate of protein degradation than the rate of protein synthesis [1]. Protein degradation is caused by autophagy and the ubiquitin proteasome system [1]. Autophagy is a process that naturally breaks down unnecessary or nonfunctional cell components, resulting in the formation of autophagosomes. The resulting autophagosomes and lysosomes are fused and decomposed [2]. In the ubiquitin proteasome system, a proteasome recognizes and decomposes misfolded or unnecessary proteins attached to ubiquitin. Muscle-specific ligases include muscle ring finger 1 (MuRF1) and muscle atrophy F box (Atrogin-1). Their overexpression is known to promote muscle atrophy [3]. Myostatin regulates the expression of MuRF-1 and Atrogin-1 [4]. Inhibiting the expression of myostatin causes muscles to become hypertrophic.

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