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
YT Tseng, WH Chang, CC Lin, FR Chang, PC Wu
Lab
College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
Journal
Phytomedicine
Abstract
In C2C12 myotubes, LWDH-WE attenuated MG-induced cellular death and oxidative damage accompanied with improving mitochondrial membrane potential, inhibiting NADPH oxidase (Nox) activation, and ROS production. Moreover, LWDH-WE could attenuate MG-induced atrophy of C2C12 myotubes accompanied with regulating protein synthesis (IGF-1R, Akt, mTOR) and protein degradation (FoxO3a, atrogin-1, MuRF-1) signals. In STZ-induced diabetic mice, LWDH-WE improved body weight and skeletal muscle mass of mice. LWDH-WE also enhanced muscle strength of STZ-induced diabetic mice. Furthermore, LWDH-WE enhanced the improvement of insulin on gastrocnemius muscle mass and grip strength in STZ-treated mice.
BIOSEB Instruments Used:
Grip strength test (BIO-GS3)
