Tenuigenin ameliorates acute lung injury by inhibiting NF-κB and MAPK signalling pathways

• TNG decreased the production of TNF-α, IL-1β, and IL-6 in vitro.
• TNG attenuated pulmonary damage in LPS-induced ALI model.
• TNG decreased lung inflammatory response to LPS in ALI model.
• TNG blocked MAPKs and NF-κB pathways activation in LPS-induced ALI model.

We aimed to explore the protective effect of tenuigenin (TNG) on lipopolysaccharide (LPS)-stimulated inflammatory responses in acute lung injury (ALI). Thus, we assessed the effects of TNG on the LPS-induced production of tumour necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in the culture supernatants of RAW 264.7 cells. Male BALB/c mice were pretreated with commercial TNG (2, 4 and 8 mg/kg) and dexamethasone (Dex, 5 mg/kg) for 1 h prior to LPS (0.5 mg/kg) challenge. After 12 h, airway inflammation was assessed. Our results showed that TNG dramatically decreased the production of TNF-α, IL-1β, and IL-6 in vitro and in vivo as well as the expression of COX-2 protein in vivo. Treatment with TNG not only significantly ameliorated LPS-stimulated histopathological changes but also reduced the myeloperoxidase (MPO) activity and the wet-to-dry weight ratio of the lungs. Furthermore, TNG blocked IκBα phosphorylation and degradation and inhibited p38/ERK phosphorylation in LPS-induced ALI. These findings suggest that TNG may have a protective effect on LPS-induced ALI and may be useful for the prevention and treatment of ALI in the clinical setting.

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