| First Author | Tao W | Year | 2018 |
| Journal | Shock | Volume | 50 |
| Issue | 5 | Pages | 589-594 |
| PubMed ID | 29206762 | Mgi Jnum | J:302893 |
| Mgi Id | MGI:6510913 | Doi | 10.1097/SHK.0000000000001067 |
| Citation | Tao W, et al. (2018) Soluble Epoxide Hydrolase Plays a Vital Role in Angiotensin II-Induced Lung Injury in Mice. Shock 50(5):589-594 |
| abstractText | BACKGROUND: Angiotensin II plays a vital role in the pathogenesis of acute respiratory distress syndrome (ARDS). However, its mechanism is not well defined. Angiotensin II upregulates the expression of soluble epoxide hydrolase (sEH; Ephx2). sEH is suggested as a potential pharmacologic target for ARDS. The present study investigates whether the sEH is involved in the angiotensin II-triggered pulmonary inflammation and edema using an angiotensin II-induced lung injury animal model. METHODS: Lung injury was induced by angiotensin II intratracheally instillation in wild-type or Ephx2 deficient mice. RESULTS: sEH activities were markedly increased in wild-type mice treated with angiotensin II. Angiotensin II markedly increased the levels of tumor necrosis factor-alpha and interleukin-1beta in bronchoalveolar lavage fluid, worsened alveolar capillary protein leak and lung histological alterations, and elevated activity of activator protein-1 and nuclear factor-kappaB. However, these changes were significantly improved in Ephx2 deficient mice. Moreover, Losartan, an angiotensin II receptor 1 antagonist, abolished the sEH induction and improved mortality. CONCLUSIONS: Angiotensin II-induced lung injury was improved in sEH gene deleted mice. The angiotensin II-triggered pulmonary inflammation is mediated, at least in part, through the sEH. |
