PMID- 28503033
OWN - NLM
STAT- MEDLINE
DCOM- 20180309
LR  - 20181113
IS  - 1466-1861 (Electronic)
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 2017
DP  - 2017
TI  - 15-Deoxy-Delta(12,14)-prostaglandin J(2) Exerts Antioxidant Effects While 
      Exacerbating Inflammation in Mice Subjected to Ureteral Obstruction.
PG  - 3924912
LID - 10.1155/2017/3924912 [doi]
LID - 3924912
AB  - Urinary obstruction is associated with inflammation and oxidative stress, leading 
      to renal dysfunction. Previous studies have shown that 
      15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) has both antioxidant and 
      anti-inflammatory effects. Using a unilateral ureteral obstruction (UUO) mouse 
      model, we examined the effects of 15d-PGJ(2) on oxidative stress and inflammation 
      in the kidney. Mice were subjected to UUO for 3 days and treated with 15d-PGJ(2). 
      Protein and RNA expression were examined using immunoblotting and qPCR. 
      15d-PGJ(2) increased NF-E2-related nuclear factor erythroid-2 (Nrf2) protein 
      expression in response to UUO, and heme oxygenase 1 (HO-1), a downstream target 
      of Nrf2, was induced by 15d-PGJ(2). Additionally, 15d-PGJ(2) prevented protein 
      carbonylation, a UUO-induced oxidative stress marker. Inflammation, measured by 
      nuclear NF-kappaB, F4/80, and MCP-1, was increased in response to UUO and further 
      increased by 15d-PGJ(2). Renal injury was aggravated by 15d-PGJ(2) treatment as 
      measured by kidney injury molecule-1 (KIM-1) and cortical caspase 3 content. No 
      effect of 15d-PGJ(2) was observed on renal function in mice subjected to UUO. 
      This study illustrates differentiated functioning of 15d-PGJ(2) on inflammation 
      and oxidative stress in response to obstructive nephropathy. High concentrations 
      of 15d-PGJ(2) protects against oxidative stress during 3-day UUO in mice; 
      however, it aggravates the associated inflammation.
FAU - Nilsson, Line
AU  - Nilsson L
AD  - Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
FAU - Palm, Fredrik
AU  - Palm F
AD  - Division of Integrative Physiology, Department of Medical Cell Biology, Uppsala 
      University, Uppsala, Sweden.
AD  - Division of Drug Research, Department of Medical Health Sciences, Linkoping 
      University, Linkoping, Sweden.
FAU - Norregaard, Rikke
AU  - Norregaard R
AUID- ORCID: 0000-0002-1287-4181
AD  - Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (15-deoxyprostaglandin J2)
RN  - 0 (Antioxidants)
RN  - 0 (Havcr1 protein, mouse)
RN  - 0 (Hepatitis A Virus Cellular Receptor 1)
RN  - 0 (Kelch-Like ECH-Associated Protein 1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - RXY07S6CZ2 (Prostaglandin D2)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Hepatitis A Virus Cellular Receptor 1/metabolism
MH  - Immunoblotting
MH  - Inflammation/drug therapy
MH  - Kelch-Like ECH-Associated Protein 1/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-E2-Related Factor 2/metabolism
MH  - NF-kappa B/metabolism
MH  - Prostaglandin D2/*analogs & derivatives/pharmacology
MH  - Protein Carbonylation/drug effects
MH  - Signal Transduction
MH  - Ureteral Obstruction/*drug therapy
PMC - PMC5414590
EDAT- 2017/05/16 06:00
MHDA- 2018/03/10 06:00
PMCR- 2017/04/19
CRDT- 2017/05/16 06:00
PHST- 2016/11/28 00:00 [received]
PHST- 2017/02/17 00:00 [revised]
PHST- 2017/03/12 00:00 [accepted]
PHST- 2017/05/16 06:00 [entrez]
PHST- 2017/05/16 06:00 [pubmed]
PHST- 2018/03/10 06:00 [medline]
PHST- 2017/04/19 00:00 [pmc-release]
AID - 10.1155/2017/3924912 [doi]
PST - ppublish
SO  - Mediators Inflamm. 2017;2017:3924912. doi: 10.1155/2017/3924912. Epub 2017 Apr 
      19.