PMID- 29997937
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230926
IS  - 2072-1439 (Print)
IS  - 2077-6624 (Electronic)
IS  - 2072-1439 (Linking)
VI  - 10
IP  - 5
DP  - 2018 May
TI  - Pyrroloquinoline quinone attenuates cachexia-induced muscle atrophy via 
      suppression of reactive oxygen species.
PG  - 2752-2759
LID - 10.21037/jtd.2018.04.112 [doi]
AB  - BACKGROUND: Cachexia, a wasting syndrome, is most commonly observed in 
      individuals with advanced cancer including lung cancer, esophageal cancer, liver 
      cancer, etc. The characteristic sign of cachexia is muscle atrophy. To date, 
      effective countermeasures have been still deficiency to alleviate muscle atrophy. 
      Reactive oxygen species (ROS) are important regulators of muscle atrophy. 
      Therefore, the effects of a naturally antioxidant, pyrroloquinoline quinone 
      (PQQ), were explored on muscle atrophy induced by cachexia in the present study. 
      METHODS: Tumor necrosis factor-alpha (TNF-alpha) induced C2C12 myotubes atrophy model was 
      constructed. The atrophied C2C12 myotubes were dealt with the presence or absence 
      of N-acetyl-L-cysteine (NAC, an antioxidant for ROS abolition) (5 mM) or PQQ (80 
      microM) for 24 hours. ROS content was determined by dichlorodihydrofluorescein 
      diacetate (DCFH-DA) staining. The diameter of myotubes was analyzed by myosin 
      heavy chain (MHC) staining. The protein levels of MHC, muscle atrophy F-box 
      (MAFbx) and muscle RING finger-1 (MuRF-1) in each group were observed by Western 
      blotting. RESULTS: First, ROS generation was enhanced in C2C12 myotubes treated 
      with TNF-alpha. NAC treatments significantly avoided the reduction in the diameter of 
      C2C12 myotubes, and concomitantly increased MHC levels, and decreased ROS 
      contents, MuRF1 and MAFbx levels. These data suggested that the increased ROS 
      induced by TNF-alpha might play a central role in muscle wasting. PQQ (a naturally 
      occurring antioxidant) administration inhibited C2C12 myotubes atrophy induced by 
      TNF-alpha, as evidenced by the increase of the diameter of C2C12 myotubes, together 
      with increased MHC levels and decreased ROS, MAFbx and MuRF-1 levels. 
      CONCLUSIONS: PQQ resists atrophic effect dependent on, at least in part, 
      decreased ROS in skeletal muscle treated with TNF-alpha.
FAU - Xu, Tongtong
AU  - Xu T
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
AD  - School of Medicine, Nantong University, Nantong 226001, China.
FAU - Yang, Xiaoming
AU  - Yang X
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
FAU - Wu, Changyue
AU  - Wu C
AD  - School of Medicine, Nantong University, Nantong 226001, China.
FAU - Qiu, Jiaying
AU  - Qiu J
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
FAU - Fang, Qingqing
AU  - Fang Q
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
FAU - Wang, Lingbin
AU  - Wang L
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
FAU - Yu, Shu
AU  - Yu S
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
FAU - Sun, Hualin
AU  - Sun H
AD  - Laboratory of Neuroregeneration, Jiangsu Clinical Medicine Center of Tissue 
      Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, 
      Nantong University, Nantong 226001, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Thorac Dis
JT  - Journal of thoracic disease
JID - 101533916
PMC - PMC6006103
OTO - NOTNLM
OT  - Pyrroloquinoline quinone (PQQ)
OT  - muscle atrophy
OT  - oxidative stress
COIS- Conflicts of Interest: The authors have no conflicts of interest to declare.
EDAT- 2018/07/13 06:00
MHDA- 2018/07/13 06:01
PMCR- 2018/05/01
CRDT- 2018/07/13 06:00
PHST- 2018/07/13 06:00 [entrez]
PHST- 2018/07/13 06:00 [pubmed]
PHST- 2018/07/13 06:01 [medline]
PHST- 2018/05/01 00:00 [pmc-release]
AID - jtd-10-05-2752 [pii]
AID - 10.21037/jtd.2018.04.112 [doi]
PST - ppublish
SO  - J Thorac Dis. 2018 May;10(5):2752-2759. doi: 10.21037/jtd.2018.04.112.