原著和名: サンゴジュスズメウリ科名: ウリ科 = Cucurbitaceae採集地: 鹿児島県 与論島 (大隅 与論島)採集日: 1971/12/25採集者: 萩庭丈壽整理番号: JH023381国立科学博物館整理番号: TNS-VS-97338

Liu-Qing Yang (1988794)

Ping-Song Li (3142419)

Wei Tao (410556)

Yong-Bo Ma (3142416)

PLoS ONE

PubMed

Alterations of epoxyeicosatrienoic acids (EETs) (a), or soluble epoxide hydrolase (sEH) activity (b), and nuclear factor (NF)-κB activity (c) in control or lipopolysaccharide (LPS)-challenged animals treated with vehicle or AUDA. Data are expressed as the mean±SEM (n = 6~8) and compared by one-way analysis of variance and the Student-Newman-Keuls method. * P0.05 when compared with control group; † P<0.05 when compared with vehicle group. PBS, phosphate buffered saline.</p

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Effects of a Soluble Epoxide Hydrolase Inhibitor on Lipopolysaccharide-Induced Acute Lung Injury in Mice - Fig 4

Alterations of pulmonary microvascular albumin-permeability (a), or the partial pressure of arterial oxygen (PaO2)/fraction of inspired O2 (FiO2) ratio (b), myeloperoxidase (MPO) activity (c) of control or lung injury animals treated with vehicle or AUDA 24 h after lipopolysaccharide (LPS) or phosphate buffered saline (PBS) challenged. Data are expressed as the mean±SEM (n = 6~8) and compared by one-way analysis of variance and the Student-Newman-Keuls method. * P0.05 when compared with control group; † P<0.05 when compared with vehicle group.</p

Effects of a Soluble Epoxide Hydrolase Inhibitor on Lipopolysaccharide-Induced Acute Lung Injury in Mice - Fig 1

Inflammation plays a key role in the pathogenesis of acute lung injury (ALI). Soluble epoxide hydrolase (sEH) is suggested as a vital pharmacologic target for inflammation. In this study, we determined whether a sEH inhibitor, AUDA, exerts lung protection in lipopolysaccharide (LPS)-induced ALI in mice.Male BALB/c mice were randomized to receive AUDA or vehicle intraperitoneal injection 4 h after LPS or phosphate buffered saline (PBS) intratracheal instillation. Samples were harvested 24 h post LPS or PBS administration.AUDA administration decreased the pulmonary levels of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α. Improvement of oxygenation and lung edema were observed in AUDA treated group. AUDA significantly inhibited sEH activity, and elevated epoxyeicosatrienoic acids (EETs) levels in lung tissues. Moreover, LPS induced the activation of nuclear factor (NF)-κB was markedly dampened in AUDA treated group.Administration of AUDA after the onset of LPS-induced ALI increased pulmonary levels of EETs, and ameliorated lung injury. sEH is a potential pharmacologic target for ALI

Wei Tao

Ping-Song Li

Liu-Qing Yang

Yong-Bo Ma

Directory of Open Access Journals

Effects of a Soluble Epoxide Hydrolase Inhibitor on Lipopolysaccharide-Induced Acute Lung Injury in Mice.

Alterations of monocyte chemoattractant protein (MCP)-1 levels (a), or tumor necrosis factor (TNF)-α levels (b), and histopathologic scoring (c) in control or lipopolysaccharide (LPS)-challenged animals treated with vehicle or AUDA. Data are expressed as the mean±SEM (n = 6~8) and compared by one-way analysis of variance and the Student-Newman-Keuls method or Kruskal-Wallis one-way analysis of variance on ranks and the Student-Newman-Keuls method. * P0.05 when compared with control group; † P<0.05 when compared with vehicle group. PBS, phosphate buffered saline.</p

Effects of a Soluble Epoxide Hydrolase Inhibitor on Lipopolysaccharide-Induced Acute Lung Injury in Mice - Fig 3

https://figshare.com/articles/Effects_of_a_Soluble_Epoxide_Hydrolase_Inhibitor_on_Lipopolysaccharide-Induced_Acute_Lung_Injury_in_Mice_-_Fig_1/3870729

Melothria maderaspatana Cogn.

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