Allicin attenuates lipopolysaccharideinduced acute lung injury in neonatal rats via the PI3K/Akt pathway

Allicin is an oxygenated carotenoid derivative that exhibits strong antioxidant activity, which effectively removes reactive oxygen species from the body and has important roles in disease prevention and treatment. Therefore, the present study aimed to investigate whether allicin attenuates lipopolysaccharide (LPS)induced acute lung injury (ALI) in neonatal rats and the potential underlying mechanisms. An LPSinduced ALI neonatal rat model was utilized to assess the therapeutic value and mechanisms of allicin. Following allicin treatment, increases in lung wet/dry ratio and the lung protein concentration were significantly suppressed in LPSinduced ALI neonatal rats. Furthermore, ELISA results demonstrated that allicin significantly reduced the levels of malondialdehyde, tumor necrosis factorα and interleukin6, and increased superoxide dismutase activity, in the bronchoalveolar lavage fluid of LPStreated rats. Additionally, allicin administration increased the protein expression of Bcl2 and reduced the activity of caspase3/-9, as determined by western blotting or ELISA, respectively, and increased phosphatidylinositol 3kinase (PI3K) and phosphorylatedAkt protein levels, in LPStreated ALI neonatal rats. The results of the present study indicate that allicin attenuate LPSinduced ALI in neonatal rats by ameliorating oxidative stress, inflammation and apoptosis via the PI3K/Akt pathway. Allicin may be used for development of a novel drug for treatment of ALI.