Related Experiment Video
Updated: May 22, 2025

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells
Published on: December 11, 2020
Melatonin Alleviates Oxidative Stress-Induced Mitochondrial Dysfunction Through Ameliorating NAD+ Homeostasis of
Xiu Peng1, Li Zhao1, Jiale Wang1
1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.
Abstract:
Human dental pulp stem cells (hDPSCs) exhibit amazing therapeutic abilities in a variety of diseases due to their remarkable self-renewal capacity and multi-differentiation potential. However, their therapeutic potential could be weakened by various factors such as oxidative stress in cell survival microenvironment In Vivo. Here, we explored the protective effect and mechanism of melatonin (Mel) on hDPSCs transplanted in a type 1 diabetes mellitus (T1DM) rat model. Nicotinamide adenine dinucleotide (NAD+) metabolism and mitochondrial function were remarkably impaired in T1DM rats caused by oxidative stress, while the combination of Mel and post-hDPSCs transplantation could rebalance NAD+ homeostasis through regulating NAMPT-NAD+-SIRT1 axis. Furthermore, Mel significantly reduced intracellular and mitochondrial reactive oxygen species, and alleviated cell senescence and apoptosis of hDPSCs exposed to hydrogen peroxide through ameliorating NAD+ depletion and mitochondrial dysfunction. The protective role of Mel could be extremely essential to stem cells in tissue engineering and regenerative medicine.
Related Concept Videos
Mitochondrial Membranes
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Mitochondria
Insufficient Sleep and Sleep Deprivation
Sleep deprivation is a more severe form of sleep loss...
Management of Insomnia

