Activity, Motor Control & Coordination
Pain - Thermal Allodynia / Hyperalgesia
Pain - Spontaneous Pain - Postural Deficit
Pain - Mechanical Allodynia / Hyperalgesia
Anxiety & Depression Disorder
Learning/Memory - Attention - Addiction
Physiology & Respiratory Research
Metabolism - Food & Drink Intake
Pain
Central Nervous System (CNS)
Neurodegeneration
Sensory system
Motor control
Mood Disorders
Other disorders
Muscular system
Joints
Metabolism
Cross-disciplinary subjects
SFN2024: Meet our team in Chicago on booth #876 Authors
YS Hah, KH Cho, EJ Kim, YH Son, JH Lee et al
Lab
Department of Orthopedic Surgery, Gyeongsang National University School of Medicine and Biomedical Research Institute, Gyeongsang National University Hospital, Gyeongnam, Korea
Journal
ResearchGate
Abstract
Glucocorticoids (GCs) are negative muscle protein regulators that cause muscle atrophy when used in high doses or after the sustained use of GCs in numerous pathological conditions. Thus, the development of a treatment for GC-induced muscle atrophy has clinical importance. Some natural products effectively prevent muscle loss in several muscle atrophy conditions. Green tea extract (GTE) has a broad range of health benefits, including liver injury, but its effects on muscle atrophy are unclear. In this study, GTE was isolated from different extraction processes, and the protective effect of GTE on dexamethasone (Dexa)-induced atrophy was investigated in C2C12 myotubes and C57BL/6 mice. In vitro experiments were conducted using the Dexa-induced atrophy in cultured C2C12 myotubes and were evaluated by the expression of muscle atrophy F-box (MAFbx) and MyoD using real-time PCR and western blots. Muscle dysfunction was established in male C57BL/6 mice (eight weeks old, n=6) treated with a relatively high dose of Dexa (10 mg/kg body weight, i.p., 14 days). The body weight, grip strength, treadmill test, muscle weight, and muscle histology were assessed. GTE preserved Dexa-induced muscle atrophy in C2C12 myotubes, as indicated by the decreased expression of MAFbx. In Dexa-induced muscle wasting C57BL/6 mice, the 1000 mg/kg GTE treatment rescued Dexa-induced muscle weakness, as indicated by the prolonged running exhaustive time and improved grip strength. GTE also preserved the muscles from gastrocnemius and tibialis anterior muscle mass and muscle fiber cross-sectional area losses. These results suggest that GTE ameliorates Dexa-induced skeletal muscle wasting by regulating MAFbx, which might be developed as a therapeutic agent for the treatment of muscle atrophy and weakness.
BIOSEB Instruments Used:
Grip strength test (BIO-GS3)
