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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Protective effect of pterostilbene on sepsis-induced acute lung injury in a rat model via the JAK2/STAT3 pathway
1Xi'an Jiaotong University Health Science Center, Xi'an, China.
Background:
Bacterial infection is one of the most common causes of sepsis, with acute lung injury (ALI) being a related complication. Pterostilbene (PTS) is extracted from blueberries, peanuts, and grapes, and has numerous pharmacologic activities. The aim of the present study was to explore the underlying role of PTS protects against sepsis-mediated ALI.
Methods:
We established a sepsis model induced by cecal ligation and puncture (CLP) in rats. The rats were randomly divided into five groups (n=5 each): sham group, CLP group, Dexmedetomidine group (Dex, 50 µg/kg) and PTS groups (25 and 50 mg/kg). Twenty-hours hours after CLP, PTS was intraperitoneally injected for 14 continuous days. The rats were killed, and blood and lung tissue were collected for pathological analysis and mRNA and protein detection.
Results:
Our findings showed that PTS reduced the wet/dry ratio and ameliorated sepsis-induced pulmonary fibrosis (PF), which was associated with improvement of pathological damage in lung tissues. We also observed the inhibitory effect of PTS on apoptosis and release of inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-6, and monocyte chemotactic protein 1). In addition, PTS markedly suppressed the phosphorylation levels of Janus kinase-2 (JAK2) and signal transducer and activator of transcription 3 (STAT3).
Conclusions:
Our results indicated that PTS inhibited the PF, apoptosis, and inflammatory response via the JAK2/STAT3 pathway in a sepsis-induced ALI rat model, providing a candidate for drug therapy of sepsis-induced ALI.
