PMID- 25647402
OWN - NLM
STAT- MEDLINE
DCOM- 20151123
LR  - 20181113
IS  - 1535-4989 (Electronic)
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 53
IP  - 3
DP  - 2015 Sep
TI  - Enhanced Resolution of Hyperoxic Acute Lung Injury as a result of Aspirin 
      Triggered Resolvin D1 Treatment.
PG  - 422-35
LID - 10.1165/rcmb.2014-0339OC [doi]
AB  - Acute lung injury (ALI), which presents as acute respiratory failure, is a major 
      clinical problem that requires aggressive care, and patients who require 
      prolonged oxygen exposure are at risk of developing this disease. Although 
      molecular determinants of ALI have been reported, the molecules involved in 
      disease catabasis associated with oxygen toxicity have not been well studied. It 
      has been reported that lung mucosa is rich in omega-3 fatty acid dicosahexanoic 
      acid (DHA), which has antiinflammatory properties. Aspirin-triggered resolvin D1 
      (AT-RvD1) is a potent proresolution metabolite of DHA that can curb the 
      inflammatory effects in various acute injuries, yet the effect of AT-RvD1 on 
      hyperoxic acute lung injury (HALI) or in the oxygen toxicity setting in general 
      has not been investigated. The effects of AT-RvD1 on HALI were determined for the 
      first time in 8- to 10-week-old C57BL/6 mice that were exposed to hyperoxia (>/=95% 
      O2) for 48 hours. Mice were given AT-RvD1 (100 ng) in saline or a saline vehicle 
      for 24 hours in normoxic ( approximately 21% O2) conditions after hyperoxia. Lung tissue and 
      bronchoalveolar lavage (BAL) fluid were collected for analysis associated with 
      proinflammatory signaling and lung inflammation. AT-RvD1 treatment resulted in 
      reduced oxidative stress, increased glutathione production, and significantly 
      decreased tissue inflammation. AT-RvD1 treatment also significantly reduced the 
      lung wet/dry ratio, protein in BAL fluid, and decreased apoptotic and NF-kappaB 
      signaling. These results show that AT-RvD1 curbs oxygen-induced lung edema, 
      permeability, inflammation, and apoptosis and is thus an effective therapy for 
      prolonged hyperoxia exposure in this murine model.
FAU - Cox, Ruan Jr
AU  - Cox R Jr
AD  - Departments of 1 Internal Medicine and.
AD  - 2 Molecular Medicine, Division of Allergy and Immunology, Morsani College of 
      Medicine, University of South Florida, Tampa, Florida.
FAU - Phillips, Oluwakemi
AU  - Phillips O
AD  - Departments of 1 Internal Medicine and.
FAU - Fukumoto, Jutaro
AU  - Fukumoto J
AD  - Departments of 1 Internal Medicine and.
FAU - Fukumoto, Itsuko
AU  - Fukumoto I
AD  - Departments of 1 Internal Medicine and.
FAU - Parthasarathy, Prasanna Tamarapu
AU  - Parthasarathy PT
AD  - Departments of 1 Internal Medicine and.
FAU - Arias, Stephen
AU  - Arias S
AD  - Departments of 1 Internal Medicine and.
FAU - Cho, Young
AU  - Cho Y
AD  - Departments of 1 Internal Medicine and.
FAU - Lockey, Richard F
AU  - Lockey RF
AD  - Departments of 1 Internal Medicine and.
FAU - Kolliputi, Narasaiah
AU  - Kolliputi N
AD  - Departments of 1 Internal Medicine and.
AD  - 2 Molecular Medicine, Division of Allergy and Immunology, Morsani College of 
      Medicine, University of South Florida, Tampa, Florida.
LA  - eng
GR  - R01 HL105932/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (resolvin D1)
RN  - 25167-62-8 (Docosahexaenoic Acids)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Acute Lung Injury/*drug therapy/immunology/metabolism
MH  - Airway Resistance
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - Apoptosis
MH  - Aspirin/*pharmacology
MH  - Docosahexaenoic Acids/*physiology
MH  - Drug Evaluation, Preclinical
MH  - Hyperoxia/*drug therapy/metabolism
MH  - Lung/immunology/metabolism/pathology
MH  - Mice, Inbred C57BL
MH  - Neutrophil Infiltration
MH  - Oxidative Stress
PMC - PMC4566067
OTO - NOTNLM
OT  - acute lung injury
OT  - hyperoxia
OT  - resolvin
EDAT- 2015/02/04 06:00
MHDA- 2015/12/15 06:00
PMCR- 2016/09/01
CRDT- 2015/02/04 06:00
PHST- 2015/02/04 06:00 [entrez]
PHST- 2015/02/04 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
PHST- 2016/09/01 00:00 [pmc-release]
AID - 10.1165/rcmb.2014-0339OC [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2015 Sep;53(3):422-35. doi: 10.1165/rcmb.2014-0339OC.