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 anti-oxidant 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-κB,we concluded Taxifolin suppresses oxidative stress and inflammation in B[a]P induced lung injury possibly via stimulating the Nrf2 signaling pathway.