Protective effects of dietary luteolin against mercuric chloride-induced lung injury in mice: Involvement of AKT/Nrf2 and NF-κB pathways

Food-derived compound luteolin possesses multiple pharmacological activities. Accordingly, we focused on exploring the protective effects of luteolin (100 mg/kg) against mercuric chloride (HgCl2) (5 mg/kg) stimulated lung injury and the molecular mechanisms of lung protection effects in mouse. The influence of luteolin on histologic changes, oxidative stress, proinflammatory cytokine production, neutrophil activation, and apoptosis were assayed in HgCl2-induced lung injury. Luteolin administration attenuated pulmonary histologic conditions and apoptotic change. The protective effects of luteolin might be attributed to the reduction of myeloperoxidase, inflammatory cytokines, malondialdehyde, and the increase of superoxide dismutase and glutathione. Luteolin promoted protein kinase B (AKT) phosphorylation and translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) into nucleus, and inhibited activation of nuclear factor kappa B (NF-κB) in HgCl2-induced lung injury. Taken together, dietary luteolin may be an effective candidate for treatment of HgCl2-induced lung injury by preventing NF-κB activation and activating AKT/Nrf2 pathway. [Display omitted] •Luteolin protects against the lung injury induced by mercuric chloride (HgCl2).•HgCl2-induced lung injury is characterized by oxidative stress and the activation of NF-κB.•Luteolin activates AKT/Nrf2 signaling axis and inhibits NF-κB activation in HgCl2-induced lung injury.