Related Experiment Video
Updated: Aug 19, 2025
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Ginsenoside Rb1 Prevents Oxidative Stress-Induced Apoptosis and Mitochondrial Dysfunction in Muscle Stem Cells via
Wenxi Dong1,2, Wenhao Chen1,2, Hongbo Zou1,3
1Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Abstract:
Sarcopenia, featured by the progressive loss of skeletal muscle function and mass, is associated with the impaired function of muscle stem cells (MuSCs) caused by increasing oxidative stress in senescent skeletal muscle tissue during aging. Intact function of MuSCs maintains the regenerative potential as well as the homeostasis of skeletal muscle tissues during aging. Ginsenoside Rb1, a natural compound from ginseng, exhibited the effects of antioxidation and against apoptosis. However, its effects of restoring MuSC function during aging and improving age-related sarcopenia remained unknown. In this study, we investigated the role of Rb1 in improving MuSC function and inhibiting apoptosis by reducing oxidative stress levels. We found that Rb1 inhibited the accumulation of reactive oxygen species (ROS) and protected the cells from oxidative stress to attenuate the H2O2-induced cytotoxicity. Rb1 also blocked oxidative stress-induced apoptosis by inhibiting the activation of caspase-3/9, which antagonized the decrease in mitochondrial content and the increase in mitochondrial abnormalities caused by oxidative stress via promoting the protein expression of genes involved in mitochondrial biogenesis. Mechanistically, it was proven that Rb1 exerted its antioxidant effects and avoided the apoptosis of myoblasts by targeting the core regulator of the nuclear factor-kappa B (NF-κB) signal pathway. Therefore, these findings suggest that Rb1 may have a beneficial role in the prevention and treatment of MuSC exhaustion-related diseases like sarcopenia.
Insights
Ginsenoside Rb1 combats aging-related muscle loss (sarcopenia) by protecting muscle stem cells (MuSCs) from oxidative stress and apoptosis. This natural compound restores mitochondrial function and may prevent diseases linked to MuSC exhaustion.
Area of Science:
- Gerontology
- Cell Biology
- Biochemistry
Background:
- Sarcopenia, age-related muscle loss, is linked to impaired muscle stem cell (MuSC) function due to oxidative stress.
- Maintaining MuSC function is crucial for skeletal muscle regeneration and homeostasis during aging.
Purpose of the Study:
- To investigate the potential of Ginsenoside Rb1 in restoring aged MuSC function and mitigating sarcopenia.
- To determine if Rb1 can reduce oxidative stress and inhibit apoptosis in MuSCs.
Main Methods:
- Assessed Rb1's effects on reactive oxygen species (ROS) accumulation and hydrogen peroxide (H2O2)-induced cytotoxicity.
- Evaluated Rb1's impact on oxidative stress-induced apoptosis, caspase-3/9 activation, and mitochondrial parameters.
- Investigated Rb1's mechanism of action, focusing on the nuclear factor-kappa B (NF-κB) signaling pathway.
Main Results:
- Rb1 inhibited ROS accumulation and protected cells from oxidative stress, attenuating H2O2-induced damage.
- Rb1 blocked apoptosis by inhibiting caspase-3/9 activation and preserved mitochondrial content and function.
- Rb1 promoted mitochondrial biogenesis gene expression, counteracting oxidative stress-induced mitochondrial dysfunction.
- Rb1's antioxidant and anti-apoptotic effects were mediated through targeting the NF-κB pathway.
Conclusions:
- Ginsenoside Rb1 demonstrates significant antioxidant and anti-apoptotic properties relevant to muscle stem cell health.
- Rb1 shows promise in preventing and treating sarcopenia and other diseases associated with MuSC exhaustion.
More Related Videos
07:40Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
08:00Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
Published on: July 10, 2019
