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

Respir Physiol Neurobiol

College of Veterinary Medicine, Jilin University, Changchun 130062, PR China; Institutes of Translational Medicine, The First Hospital, Jilin University, Changchun 130001, PR China. Electronic address:

Published: September 2015

AI Article Synopsis

  • The study investigated how tenuigenin (TNG) can protect against inflammation caused by lipopolysaccharide (LPS) in acute lung injury (ALI) using both cell cultures and male BALB/c mice.
  • TNG significantly reduced the levels of inflammatory markers such as TNF-α, IL-6, and IL-1β, as well as improved lung histopathology and reduced lung injury indicators like myeloperoxidase activity.
  • The research indicates that TNG may inhibit specific inflammatory pathways, suggesting its potential as a therapeutic option for treating ALI in clinical scenarios.

Article Abstract

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, 5mg/kg) for 1h prior to LPS (0.5 mg/kg) challenge. After 12h, 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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http://dx.doi.org/10.1016/j.resp.2015.04.010DOI Listing

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