Kurarinone Attenuates LPS-Induced Pneumonia by Inhibiting MAPK and NF-κB Signaling Pathways

Abstract

Kurarinone is a prenylated flavanone isolated from Sophora flavescens Aiton. This investigation aimed to elucidate whether kurarinone could ameliorate lipopolysaccharide (LPS)-induced pneumonia and explore the underlying mechanism. C57BL/6 mice were treated with LPS (50 μg/20 μL) to establish pneumonia models. Kurarinone (100 mg/kg) or dexamethasone (DEX, 5 mg/kg) was administered for 7 days before LPS inhalation. BEAS-2B cells were incubated with kurarinone at 1, 2, and 5 μM for 2 h before LPS stimulation for 24 h. We found that kurarinone ameliorated lung injury and inflammatory cell infiltration in the mouse lung (p < 0.001). Kurarinone decreased MPO activity (47.6%, p < 0.001) and alleviated the inflammatory response by reducing the levels of IL-1β (34.9%, p < 0.001), TNF-α (55.1%, p < 0.001), and IL-6 (36.2%, p < 0.001) in the lung. Kurarinone reduced the levels of IL-1β, TNF-α, IL-6, iNOS, and COX2 in LPS-treated BEAS-2B cells in a concentration-dependent manner (p < 0.05). Mechanistically, kurarinone restrained LPS-induced activation of MAPK and NF-κB pathways in vivo and in vitro (p < 0.05). Overall, kurarinone alleviates LPS-induced pneumonia in mice by reducing inflammation via MAPK and NF-κB pathways, suggesting that kurarinone might be a potential therapeutic agent for pneumonia. This study provides new research ideas for the discovery of natural flavonoids that can treat pneumonia.