Acrolein (2-propenal) is ubiquitous in the environment and connections exist between acrolein exposure and lung cancer risk. Here we investigated the effects of naringin on acrolein induced-lung injuries in mice. Male C57BL/6 mice were allocated into four groups: Vehicle group (no acrolein), Naringin only group (80 mg of naringin/kg bw + no acrolein), Acrolein group (ACR group; acrolein), and Naringin + Acrolein group (NAG+ACR group; 80 mg of naringin/kg bw and acrolein). The mice were subjected acute acrolein inhalation (10 ppm for 12 h) in an inhalation chamber and naringin was intraperitoneally administered to the mice one hour before acrolein exposure. The results demonstrated that, in the NAG+ACR group, pulmonary injuries (e.g., airspace enlargement, lung inflammation) were all significantly improved compared to the ACR group. Further, key markers of MAPK signaling (e.g., p-p38, p-JNK), p53 signaling markers (e.g., p-Chk2, p53), NF-κB signaling axis (e.g., IL-1 β, TNF-α), and oxidative damage markers (e.g.
, gssg: GSH ratio, oxidative DNA damage) were all effectively mitigated by the naringin treatment. Naringin provided protection against the environmental toxicant, acrolein, in mice lung via modulating MAPK, p53, and NF-κB signaling pathways and our data may provide significant implications considering the prevalence of acrolein.
Keywords: Acrolein; Apoptosis; Inflammation; Naringin; Reactive Oxygen Species.
Copyright © 2018. Published by Elsevier Inc.