Taxifolin ameliorates Benzo[a]pyrene-induced lung injury possibly via stimulating the Nrf2 signalling pathway

Benzo[a]pyrene, an environmental contaminant as well as a mutagen is widely found in cigarette smoke, automobile exhaust particles among other sources. The present study underlines the protective effect of Taxifolin on B[a]P induced lung injury in male Swiss Albino Mice by analyzing the activity/level of various pro and antioxidant parameters, Inflammatory markers, Phase II enzyme, as well as lung histology. Taxifolin was administered orally to mice at either dose of 20 or 40 mg/kg body weight for 14 days and then challenged with a single dose of B[a]P (125 mg/kg body weight by oral gavage) on the 14th day. Our results show treatment with B[a]P leads to increased activity/level of CYP450R, EH, pro-inflammatory proteins, as well as lipid peroxidation and reduce level/activity of anti-oxidant molecules while Taxifolin treatment shows ameliorative effect. Administration of B[a]P also leads to decrease in expression of ROS sensitive factor Nrf2 and its downstream target NQO1,HO-1,SOD while Taxifolin treated animals showed a very high level of expression of Nrf2,NQO1,HO-1, SOD. Since Nrf2 plays central role in providing resistance to oxidative stress and also suppresses inflammation by inhibiting NF-kappa B,we concluded Taxifolin suppresses oxidative stress and inflammation in B[a]P induced lung injury possibly via stimulating the Nrf2 signaling pathway.

Automated summary

The study highlights the protective effect of Taxifolin on Benzo[a]pyrene-induced lung injury in mice, showing that Taxifolin suppresses oxidative stress and inflammation through stimulating the Nrf2 signaling pathway.