Acute lung injury (ALI) is a serious respiratory disease characterized by pulmonary inflammatory cell infiltration and oxidative stress and is the leading cause of human death. Naringenin (NAR) is a naturally active flavonoid widely present in citrus fruits and has been shown to have multiple pharmacological effects. In this study, we evaluated the potential mechanism of NAR in lipopolysaccharide (LPS)-induced ALI by constructing a mice model of ALI. It was found that NAR significantly increased the 7-day survival rate of mice after LPS stimulation, improved lung index, tissue inflammatory infiltration, and fibrosis levels, and found that it decreased Interleukin-1 beta(IL-1β), Interleukin-6(IL-6), Tumor Necrosis Factor-alpha(TNF-α), and Malondialdehyde(MDA) levels in bronchoalveolar lavage fluid (BALF), while increasing Glutathione(GSH) and Superoxide Dismutase(SOD) levels. In addition, naringenin suppressed the expression of apoptotic proteins BCL2-Associated X Protein(BAX), Cysteine-Aspartate Protease 3(Caspase 3)and Cleaved-Caspase 3, promoted the expression of B-Cell Lymphoma 2(Bcl-2), and upregulated the expression of Nuclear Factor Erythroid 2-Related Factor 2(NRF2) and Heme Oxygenase-1(HO-1) in lung tissue. These studies suggest that naringenin ameliorates LPS-induced acute lung injury in mice by activating the NRF2/HO-1 pathway.
Keywords: NRF2/HO‐1 pathway; lung injury; naringenin; oxidative stress.
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