Abstract
Objectives: ALI is a diffuse heterogeneous lung injury characterized by hypoxemia, low lung compliance and widespread capillary leakage. The levels of oxidative stress and inflammation are very high in the lung tissue of the ALI patients. In this study, we investigated the effects of chrysin on oxidative stress and NF-κB pathway in the LPS-induced ALI model.
Methods: BALB/c mice with or without LPS intratracheally injected were intraperitonealy injected with Chrysin (50,100,200mg/kg). IL-6 and TNF-α levels in BALF were determined by ELISA. Phospho-NF-κB p65, NF-κB p65, Phospho-IκBα and IκBα levels in mouse lungs tissue were evaluated by western blot. Malondialdehyde levels in mouse lungs were detected. HE staining for histology was performed.
Results: BALF neutrophil counts,TNF-α and IL-6 levels were significantly increased in the LPS model group, but this upregulaion was attenuated by chrysin (p<0.05). And, the western blot showed us the expression levels of Phospho-NF-κB p65 were attenuated in the LPS+chrysin group compared with levels of Phospho-NF-κB p65 in the LPS Model group (p<0.05). The Malondialdehyde levels were decreased by chrysin (p<0.05). Compared with the LPS model group, the LPS+chrysin group showed less pathological changes.
Conclusions: These results suggest that chrysin attenuated oxidative stress and the levels of Phospho-NF-κB p65 induced by LPS; the inflammation was also reduced by chrysin. Chrysin might have the function to protect lungs from the LPS-induced ALI through the regulation of oxidative stress and the NF-κB pathway.
- © 2014 ERS
