Barbaloin protects against lipopolysaccharide (LPS)-induced acute lung injury by inhibiting the ROS-mediated PI3K/AKT/NF-κB pathway

Barbaloin is the major anthraquinone compound that is isolated from the leaf exudates of Aloe vera and is often used as a bittering agent in alcoholic beverages. Here, we investigated the potential protective role of barbaloin in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and clarified the underlying mechanism in vitro. Histological analysis showed that barbaloin exhibited a certain protective effect on LPS-induced ALL To further elucidate the mechanisms underlying the actions of barbaloin, LPS-stimulated macrophages were used in this study. The results showed that barbaloin decreased the phosphorylation levels of I kappa B alpha and NF-kappa B p65, leading to a reduction in the expression of pro-inflammatory cytokines (TNF-alpha, IL-1 beta and IL-6). Furthermore, barbaloin also reduced the levels of intracellular reactive oxygen species (ROS) similarly to the antioxidant N-acetyl-L-cysteine (NAC), which alone repressed the LPS-induced phosphorylation of phosphoinositide 3-kinase (PI3K) and AKT. Additionally, a pharmacological inhibitor of PI3K/AKT, LY294002, also restrained the phosphorylation levels of I kappa Ba and NF-kappa B p65 and thereby decreased the expression of pro-inflammatory cytokines. Together, these results show that barbaloin possesses a protective effect on LPS-induced ALI via suppressing the release of pro-inflammatory cytokines through the ROS-mediated PI3K/AKT/NF-kappa B pathway.