PMID- 35945990
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220811
IS  - 1178-7031 (Print)
IS  - 1178-7031 (Electronic)
IS  - 1178-7031 (Linking)
VI  - 15
DP  - 2022
TI  - Antioxidant Mitoquinone Alleviates Chronic Pancreatitis via Anti-Fibrotic and 
      Antioxidant Effects.
PG  - 4409-4420
LID - 10.2147/JIR.S357394 [doi]
AB  - BACKGROUND: Chronic pancreatitis (CP) is a long-term inflammatory disease of the 
      pancreas that can be caused by various pathogenic factors. Oxidative stress (OS), 
      which is associated with several pancreatic diseases, can induce pancreatic 
      stellate cell (PSC) activation, leading to pancreatic fibrosis. Given the 
      inefficacy of existing treatments for CP, in this study, our objective was to 
      evaluate the therapeutic effect of the antioxidant, mitoquinone (MitoQ). METHODS: 
      First, in vivo, we established a CP mouse model via the repeated injection of 
      cerulein. Mice in the MitoQ group simultaneously received MitoQ daily. After 4 
      weeks of cerulein injection, pancreatic tissues from mice were evaluated by 
      morphological changes and the expression of fibrosis markers. Further, OS in the 
      collected pancreatic tissue samples was evaluated by determining the level of 
      malondialdehyde (MDA) as well as the expression levels and activities of 
      antioxidants. Furthermore, in vitro, the effect of MitoQ on human PSCs (hPSCs) 
      was evaluated based on PSC activation markers and fibrotic phenotypes, and OS in 
      these treated hPSCs was evaluated by measuring reactive oxygen species (ROS), 
      MDA, and antioxidant levels. RESULTS: In vivo, MitoQ alleviated pancreatic 
      fibrosis and inhibited OS in the cerulein-induced murine CP model. In vitro, it 
      inhibited PSC activation as well as the subsequent development of the 
      profibrogenic phenotypes by balancing out the levels of free radicals and the 
      intracellular antioxidant system. CONCLUSION: MitoQ is a potential candidate for 
      CP treatment.
CI  - (c) 2022 Li et al.
FAU - Li, Miaomiao
AU  - Li M
AD  - Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical 
      University, Beijing, People's Republic of China.
FAU - Yuan, Yue
AU  - Yuan Y
AD  - Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical 
      University, Beijing, People's Republic of China.
FAU - Han, Xue
AU  - Han X
AD  - Department of Physiology and Pathophysiology, Peking University Health Science 
      Center, Beijing, People's Republic of China.
FAU - Liu, Xinjuan
AU  - Liu X
AD  - Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical 
      University, Beijing, People's Republic of China.
FAU - Zhang, Weizhen
AU  - Zhang W
AD  - Department of Physiology and Pathophysiology, Peking University Health Science 
      Center, Beijing, People's Republic of China.
FAU - Hao, Jianyu
AU  - Hao J
AD  - Department of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical 
      University, Beijing, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20220803
PL  - New Zealand
TA  - J Inflamm Res
JT  - Journal of inflammation research
JID - 101512684
PMC - PMC9357395
OTO - NOTNLM
OT  - MitoQ
OT  - chronic pancreatitis
OT  - mitochondria-specific antioxidant
OT  - oxidative stress
OT  - pancreatic fibrosis
OT  - pancreatic stellate cells
OT  - superoxide dismutase
COIS- The authors declare no conflicts of interest in this work.
EDAT- 2022/08/11 06:00
MHDA- 2022/08/11 06:01
PMCR- 2022/08/03
CRDT- 2022/08/10 01:48
PHST- 2022/01/07 00:00 [received]
PHST- 2022/07/04 00:00 [accepted]
PHST- 2022/08/10 01:48 [entrez]
PHST- 2022/08/11 06:00 [pubmed]
PHST- 2022/08/11 06:01 [medline]
PHST- 2022/08/03 00:00 [pmc-release]
AID - 357394 [pii]
AID - 10.2147/JIR.S357394 [doi]
PST - epublish
SO  - J Inflamm Res. 2022 Aug 3;15:4409-4420. doi: 10.2147/JIR.S357394. eCollection 
      2022.