Farrerol mitigates lipopolysaccharide-induced acute lung injury through dual regulation of oxidative stress and inflammation via Nrf2 pathway.

Acute lung injury (ALI) is a serious illness of the respiratory system that leads to lung damage. Clinical outcomes are limits and identification of a novel drug for ALI without side effects on patients. This study investigated the effects of farrerol (FRL) in a mouse model of lipopolysaccharide (LPS)-induced ALI. Mice were subjected to FRL pre-treatment 1 h prior to LPS administration daily for 7 days. Then, lung tissue was examined in various experiments, i.e. histopathology, antioxidant status, western blot and semi-quantitative polymerase chain reaction to confirm the inflammatory response in ALI experimental models. The obtained results stated that FRL treatment alleviates LPS-mediated pathological changes, such as alveolar wall thickening, decreasing lung edema, and inflammation infiltration in the lung tissue. Moreover, LPS-induced TBARS levels were modulated by FRL treatment in mice. While enhancing antioxidant enzyme activities by FRL treatment on LPS-induced mouse models. FRL also suppressed LPS-induced expression of COX-2, iNOS, TNF-α, IL-6 and IL-β1 in mouse models. In addition, FRL has a good binding interaction; therefore, it has restored the LPS-induced Nrf2 expression. These findings indicate that FRL holds a significant therapeutic agent for ALI by offering Nrf2 mediated inhibition of oxidative stress and inflammation in mouse model.