PMID- 37627571
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230828
IS  - 2076-3921 (Print)
IS  - 2076-3921 (Electronic)
IS  - 2076-3921 (Linking)
VI  - 12
IP  - 8
DP  - 2023 Aug 7
TI  - Ginsenoside Rc, an Active Component of Panax ginseng, Alleviates Oxidative 
      Stress-Induced Muscle Atrophy via Improvement of Mitochondrial Biogenesis.
LID - 10.3390/antiox12081576 [doi]
LID - 1576
AB  - Loss of skeletal muscle mass and function has detrimental effects on quality of 
      life, morbidity, and mortality, and is particularly relevant in aging societies. 
      The enhancement of mitochondrial function has shown promise in promoting muscle 
      differentiation and function. Ginsenoside Rc (gRc), a major component of ginseng, 
      has various pharmacological activities; however, its effect on muscle loss 
      remains poorly explored. In this study, we examined the effects of gRc on the 
      hydrogen peroxide (H(2)O(2))-induced reduction of cell viability in C2C12 
      myoblasts and myotubes and H(2)O(2)-induced myotube degradation. In addition, we 
      investigated the effects of gRc on the production of intracellular reactive 
      oxygen species (ROS) and mitochondrial superoxide, ATP generation, and peroxisome 
      proliferator-activated receptor-gamma co-activator 1alpha (PGC-1alpha) activity in 
      myoblasts and myotubes under H(2)O(2) treatment. Furthermore, to elucidate the 
      mechanism of action of gRc, we conducted a transcriptome analysis of myotubes 
      treated with or without gRc under H(2)O(2) treatment. gRc effectively suppressed 
      H(2)O(2)-induced cytotoxicity, intracellular ROS, and mitochondrial superoxide 
      production, restored PGC-1alpha promoter activity, and increased ATP synthesis. 
      Moreover, gRc significantly affected the expression levels of genes involved in 
      maintaining mitochondrial mass and biogenesis, while downregulating genes 
      associated with muscle degradation in C2C12 myotubes under oxidative stress. We 
      provide compelling evidence supporting the potential of gRc as a promising 
      treatment for muscle loss and weakness. Further investigations of the 
      pharmacological effects of gRc under various pathological conditions of muscle 
      loss will contribute to the clinical development of gRc as a therapeutic 
      intervention.
FAU - Kim, Aeyung
AU  - Kim A
AUID- ORCID: 0000-0002-3176-3671
AD  - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 
      Daegu 41062, Republic of Korea.
FAU - Park, Sang-Min
AU  - Park SM
AUID- ORCID: 0000-0003-2915-0742
AD  - College of Pharmacy, Chungnam National University, Daejeon 34134, Republic of 
      Korea.
FAU - Kim, No Soo
AU  - Kim NS
AUID- ORCID: 0000-0003-1437-708X
AD  - KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon 
      34054, Republic of Korea.
FAU - Lee, Haeseung
AU  - Lee H
AUID- ORCID: 0000-0002-9947-4032
AD  - College of Pharmacy and Research Institute for Drug Development, Pusan National 
      University, Busan 46241, Republic of Korea.
LA  - eng
GR  - NRF-2020R1A2C1101602, 2017R1D1A1B03034084, and 2021R1C1C1003988/National Research 
      Foundation of Korea/
GR  - Research Fund/Chungnam National University/
PT  - Journal Article
DEP - 20230807
PL  - Switzerland
TA  - Antioxidants (Basel)
JT  - Antioxidants (Basel, Switzerland)
JID - 101668981
PMC - PMC10451796
OTO - NOTNLM
OT  - ginsenoside Rc
OT  - mitochondrial biogenesis
OT  - muscle atrophy
OT  - oxidative stress
OT  - skeletal muscle
COIS- The authors declare no conflict of interest.
EDAT- 2023/08/26 10:45
MHDA- 2023/08/26 10:46
PMCR- 2023/08/07
CRDT- 2023/08/26 01:07
PHST- 2023/07/05 00:00 [received]
PHST- 2023/08/04 00:00 [revised]
PHST- 2023/08/05 00:00 [accepted]
PHST- 2023/08/26 10:46 [medline]
PHST- 2023/08/26 10:45 [pubmed]
PHST- 2023/08/26 01:07 [entrez]
PHST- 2023/08/07 00:00 [pmc-release]
AID - antiox12081576 [pii]
AID - antioxidants-12-01576 [pii]
AID - 10.3390/antiox12081576 [doi]
PST - epublish
SO  - Antioxidants (Basel). 2023 Aug 7;12(8):1576. doi: 10.3390/antiox12081576.