Licochalcone A (Lico A), a
flavonoid found in licorice root (Glycyrrhiza glabra), is known for its antimicrobial activity and its reported ability to inhibit
cancer cell proliferation. In the present study, we found that Lico A exerted potent anti-inflammatory effects in in vitro and in vivo models induced by
lipopolysaccharide (LPS). The concentrations of TNF-α,
interleukin (IL)-6, and IL-1β in the culture supernatants of RAW 264.7 cells were determined at different time points following LPS administration. LPS (0.5 mg/kg) was instilled intranasally (i.n.) in
phosphate-buffered saline to induce
acute lung injury, and 24 h after LPS was given, bronchoalveolar lavage fluid was obtained to measure pro-inflammatory mediator and total cell counts. The phosphorylation of
mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) p65
protein was analyzed by Western blotting. Our results showed that Lico A significantly reduced the amount of inflammatory cells, the
lung wet-to-dry weight (W/D) ratio,
protein leakage, and
myeloperoxidase activity and enhances
oxidase dimutase activity in mice with LPS-induced
acute lung injury (ALI).
Enzyme-linked
immunosorbent assay results indicated that Lico A can significantly down-regulate TNF-α,
IL-6, and IL-1β levels in vitro and in vivo, and treatment with Lico A significantly attenuated alveolar wall thickening, alveolar
hemorrhage, interstitial
edema, and inflammatory cells infiltration in mice with ALI. In addition, we further demonstrated that Lico A exerts an anti-
inflammation effect in an in vivo model of
acute lung injury through suppression of NF-κB activation and p38/ERK MAPK signaling in a dose-dependent manner.