PMID- 23867894
OWN - NLM
STAT- MEDLINE
DCOM- 20140304
LR  - 20211021
IS  - 1523-1747 (Electronic)
IS  - 0022-202X (Linking)
VI  - 134
IP  - 1
DP  - 2014 Jan
TI  - Hyperbaric oxygen reduces matrix metalloproteinases in ischemic wounds through a 
      redox-dependent mechanism.
PG  - 237-246
LID - S0022-202X(15)36478-2 [pii]
LID - 10.1038/jid.2013.301 [doi]
AB  - Little is known about the impact of hyperbaric oxygen treatment (HBOT) on matrix 
      metalloproteinase (MMP) production in pre-existing high-oxidant wounds. This 
      study aimed to investigate whether HBOT modulates reactive oxygen species (ROS) 
      and MMP regulation in ischemic wound tissue. Using a validated ischemic wound 
      model, Sprague-Dawley rats were divided into four groups for daily treatment: 
      HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normoxia at sea level). 
      High levels of inducible nitric oxide synthase (iNOS), gp91-phox, and 
      3-nitrotyrosine were detected in ischemic wounds, indicating high-oxidant stress. 
      HBOT not only increased antioxidant enzyme expression, such as Cu/Zn-superoxide 
      dismutase, catalase, and glutathione peroxidase, but also significantly decreased 
      pro-oxidant enzyme levels, such as iNOS and gp91-phox, thereby decreasing net 
      oxygen radical production by means of negative feedback. This effect was blocked 
      by NAC treatment in ischemic wounds. HBO-treated ischemic wounds also manifested 
      reduced phosphorylation of extracellular signal-regulated kinases 1/2, c-Jun 
      N-terminal kinase, and c-Jun, indicating downregulation of mitogen-activated 
      protein kinases (MAPKs). Furthermore, HBOT decreased the expression of several 
      MMPs while simultaneously increasing tissue inhibitor of MMP (tissue inhibitor of 
      metalloproteinase 2). These results indicate that HBOT acts via the ROS/MAPK/MMP 
      signaling axis to reduce tissue degeneration and improve ischemic wound healing.
FAU - Zhang, Qixu
AU  - Zhang Q
AD  - Plastic Surgery Department, The University of Texas MD Anderson Cancer Center, 
      Houston, Texas, USA; Plastic Surgery Division, The University of Texas Medical 
      Branch, Galveston, Texas, USA. Electronic address: lukeqixu@yahoo.com.
FAU - Gould, Lisa J
AU  - Gould LJ
AD  - Plastic Surgery Division, The University of Texas Medical Branch, Galveston, 
      Texas, USA; Department of Molecular Pharmacology and Physiology, University of 
      South Florida Morsani College of Medicine, Tampa, Florida, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130718
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Antioxidants)
RN  - 0 (Reactive Nitrogen Species)
RN  - 0 (Reactive Oxygen Species)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Antioxidants/metabolism
MH  - Catalase/metabolism
MH  - Disease Models, Animal
MH  - Hyperbaric Oxygenation/*methods
MH  - Ischemia/metabolism/*therapy
MH  - Male
MH  - Matrix Metalloproteinases/*metabolism
MH  - Nitric Oxide/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Nitrogen Species/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/physiology
MH  - Skin/*injuries/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Wound Healing/*physiology
EDAT- 2013/07/23 06:00
MHDA- 2014/03/05 06:00
CRDT- 2013/07/23 06:00
PHST- 2013/01/22 00:00 [received]
PHST- 2013/05/15 00:00 [revised]
PHST- 2013/06/06 00:00 [accepted]
PHST- 2013/07/23 06:00 [entrez]
PHST- 2013/07/23 06:00 [pubmed]
PHST- 2014/03/05 06:00 [medline]
AID - S0022-202X(15)36478-2 [pii]
AID - 10.1038/jid.2013.301 [doi]
PST - ppublish
SO  - J Invest Dermatol. 2014 Jan;134(1):237-246. doi: 10.1038/jid.2013.301. Epub 2013 
      Jul 18.