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
Preclinical studies and opioids: role in crisis management in the United States 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)
