Allicin attenuates lipopolysaccharide‑induced acute lung injury in neonatal rats via the PI3K/Akt pathway.

Abstract

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 LPS‑induced 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 LPS‑induced ALI neonatal rats. Furthermore, ELISA results demonstrated that allicin significantly reduced the levels of malondialdehyde, tumor necrosis factor‑α and interleukin‑6, and increased superoxide dismutase activity, in the bronchoalveolar lavage fluid of LPS‑treated rats. Additionally, allicin administration increased the protein expression of Bcl‑2 and reduced the activity of caspase‑3/-9, as determined by western blotting or ELISA, respectively, and increased phosphatidylinositol 3‑kinase (PI3K) and phosphorylated‑Akt protein levels, in LPS‑treated ALI neonatal rats. The results of the present study indicate that allicin attenuate LPS‑induced 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.