Protective effects of propofol on experimental neonatal acute lung injury.

The present study aimed to investigate the effects of propofol on neonatal acute lung injury (ALI) in a rat model and to examine the molecular mechanisms underlying propofol function. A rat model of ALI was established by intraperitoneal injection of lipopolysaccharides (LPS). The neonatal rats were treated with various concentrations of propofol and a lung injury score was assessed. The protein expression levels of pro‑inflammatory cytokines was detected using ELISA. In the present study, oxidative stress was determined by measuring the level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in lung tissues. Reverse transcription quantitative‑polymerase chain reaction and western blot analysis were used to examine the mRNA and protein expression levels of the factors downstream to LPS signaling pathway. Treatment with propofol significantly alleviated LPS‑induced lung injury in neonatal rats as suggested by the decreased lung injury score, increased partial pressure of oxygen and decreased lung wet‑dry weight ratio. LPS promoted the upregulation of tumor necrosis factor α (TNF‑α), interleukin (IL)‑6 and IL‑1β in lung tissues and bronchoalveolar lavage fluid from neonatal rats exhibiting ALI. Notably, treatment with propofol decreased the expression levels of these factors. Additionally, LPS caused an increase in the levels of MDA, and a decrease in SOD activity, and treatment with propofol suppressed these effects in a dose‑dependent manner. Furthermore, LPS induced the upregulation of phosphorylated (p‑)p38, nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB), p‑p65, NLR family pyrin domain containing 3 (NLRP3), apoptosis‑associated speck‑like protein containing CARD and caspase‑1 in lung tissues of neonatal rats, and treatment with propofol was able to downregulate these factors in a dose‑dependent manner. Propofol alleviated lung injury in neonatal rats with LPS‑induced ALI by preventing inflammation and oxidative stress via the regulation of the activity of the p38 mitogen‑activated protein kinase/NF‑κB signaling pathway and the expression levels of the NLRP3 inflammasome.