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Protective role of peroxisome proliferator-activated receptor β/δ in acute lung injury induced by prolonged hyperbaric hyperoxia in rats.

Abstract：

:Peroxisome proliferator-activated receptor (PPAR)-β/δ is a transcription factor that belongs to the PPAR family, but the role of PPAR-β/δ in acute lung injury (ALI) induced by hyperbaric oxygen is unknown. In this study we investigated if PPAR-β/δ activation protects from hyperoxia-induced ALI in a rat model. ALI was induced by prolonged hyperbaric oxygen (HBO2) (2.3ATA, 100% O2) for 8h. Administration of PPAR-β/δ agonist GW0742 (0.3mg/kg, i.p.) at 1 and 6h prior to HBO2 exposure significantly reduced the (1) lung injury, (2) proinflammatory cytokines (TNF-α, IL-1β, IL-6), (3) apoptosis (Bax/Bcl-2, cleaved-caspase-3 and TUNEL), (4) nuclear factor (NF)-κB expression level and DNA binding activity in the nucleus, and (5) extracellular signal-regulated kinase (ERK)1/2 phosphorylation and markedly elevated (6) superoxide dismutase and glutathione peroxidase activities as well as (7) IκB expression. However, administration of the PPAR-β/δ antagonist GSK0660 abolished these protective effects. These findings indicate that activation of PPAR-β/δ ameliorates hyperoxia-induced ALI in rats by up-regulating antioxidant enzyme activity as well as suppressing inflammation and apoptosis.

journal_name

Respir Physiol Neurobiol

journal_title

Respiratory physiology & neurobiology

authors

Bao XC,Fang YQ,You P,Zhang S,Ma J

doi

10.1016/j.resp.2014.04.004

subject

Has Abstract

pub_date

2014-08-01 00:00:00

pages

9-18

eissn

1569-9048

issn

1878-1519

pii

S1569-9048(14)00102-5

journal_volume

199

pub_type

杂志文章

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