PMID- 27753791
OWN - NLM
STAT- MEDLINE
DCOM- 20170627
LR  - 20220408
IS  - 1540-0514 (Electronic)
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 47
IP  - 5
DP  - 2017 May
TI  - Soluble Epoxide Hydrolase Inhibitor Attenuates Lipopolysaccharide-Induced Acute 
      Lung Injury and Improves Survival in Mice.
PG  - 638-645
LID - 10.1097/SHK.0000000000000767 [doi]
AB  - Acute lung injury (ALI) is characterized by rapid alveolar injury, vascular 
      leakage, lung inflammation, neutrophil accumulation, and induced cytokines 
      production leading to lung edema. The mortality rate of patients suffering from 
      ALI remains high. Epoxyeicosatrienoic acids (EETs) are cytochrome P450-dependent 
      derivatives of polyunsaturated fatty acid with antihypertensive, profibrinolytic, 
      and anti-inflammatory functions. EETs are rapidly hydrated by soluble epoxide 
      hydrolase (sEH) to their less potent diols. The aim of this study was to 
      investigate the role of sEH inhibitor trifluoromethoxyphenyl propionylpiperidin 
      urea (TPPU) and EETs in lipopolysaccharide (LPS)-induced ALI of mice. Our studies 
      revealed that inhibition of sEH with TPPU attenuated the morphological changes in 
      mice, decreased the neutrophil infiltration to the lung, pro-inflammatory 
      cytokine levels (IL-1beta and TNF-alpha) in serum and bronchoalveolar lavage fluid 
      (BALF), and alveolar capillary leakage (lung wet/dry ratio and total protein 
      concentration in BALF). TPPU improved the survival rate of LPS-induced ALI. In 
      addition, in vitro experiments revealed that both TPPU and EETs (11,12-EET and 
      14,15-EET) suppressed the expression of IL-1beta and TNF-alpha, and LDH release in 
      RAW264.7 cells. These results indicate that EETs play a role in dampening 
      LPS-induced acute lung inflammation, and suggest that sEH could be a valuable 
      candidate for the treatment of ALI.
FAU - Zhou, Yong
AU  - Zhou Y
AD  - *Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China daggerDepartment of Physiology, Hunan University of Medicine, 
      Huaihua, Hunan China double daggerDepartment of Anesthesiology, Affiliated Hospital of Zunyi 
      Medical College, Zunyi, Guizhou China  section signDepartment of Entomology and the UC Davis 
      Cancer Center, University of California Davis, Davis, California ||State Key 
      Laboratory of Trauma, Burns, and Combined Injury, Research Institute of Surgery, 
      Daping Hospital, Third Military Medical University, Chongqing, Sichuan, China.
FAU - Liu, Tian
AU  - Liu T
FAU - Duan, Jia-Xi
AU  - Duan JX
FAU - Li, Ping
AU  - Li P
FAU - Sun, Guo-Ying
AU  - Sun GY
FAU - Liu, Yong-Ping
AU  - Liu YP
FAU - Zhang, Jun
AU  - Zhang J
FAU - Dong, Liang
AU  - Dong L
FAU - Lee, Kin Sing Stephen
AU  - Lee KSS
FAU - Hammock, Bruce D
AU  - Hammock BD
FAU - Jiang, Jian-Xin
AU  - Jiang JX
FAU - Guan, Cha-Xiang
AU  - Guan CX
LA  - eng
GR  - K99 ES024806/ES/NIEHS NIH HHS/United States
GR  - R00 ES024806/ES/NIEHS NIH HHS/United States
GR  - R01 ES002710/ES/NIEHS NIH HHS/United States
GR  - U54 NS079202/NS/NINDS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 5DOQ38R4UW (11,12-epoxy-5,8,14-eicosatrienoic acid)
RN  - 81276-03-1 (14,15-epoxy-5,8,11-eicosatrienoic acid)
RN  - EC 3.3.2.- (Epoxide Hydrolases)
RN  - FC398RK06S (8,11,14-Eicosatrienoic Acid)
SB  - IM
MH  - 8,11,14-Eicosatrienoic Acid/analogs & derivatives/therapeutic use
MH  - Acute Lung Injury/chemically induced/*drug therapy/*immunology/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*therapeutic use
MH  - Epoxide Hydrolases/*antagonists & inhibitors
MH  - Interleukin-1beta/metabolism
MH  - Lipopolysaccharides/*toxicity
MH  - Mice
MH  - NF-kappa B/metabolism
MH  - Pneumonia/chemically induced/drug therapy/immunology/metabolism
MH  - RAW 264.7 Cells
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC5382142
MID - NIHMS820282
EDAT- 2016/10/19 06:00
MHDA- 2017/06/28 06:00
PMCR- 2018/05/01
CRDT- 2016/10/19 06:00
PHST- 2016/10/19 06:00 [pubmed]
PHST- 2017/06/28 06:00 [medline]
PHST- 2016/10/19 06:00 [entrez]
PHST- 2018/05/01 00:00 [pmc-release]
AID - 10.1097/SHK.0000000000000767 [doi]
PST - ppublish
SO  - Shock. 2017 May;47(5):638-645. doi: 10.1097/SHK.0000000000000767.