Lycopene mitigates atrazine-induced cardiac inflammation via blocking the NF-κB pathway and NO production

- The inflammatory response plays a role of the ATR-induced cardiac damage.
- ATR induces cardiac damage via enhancing the NO production.
- LYC shows the chemoprotective potential against ATR-induced cardiac damage.
- LYC alleviates ATR-induced cardiac damage via modulating NO-generating systems.
- LYC mitigates ATR-induced cardiac damage via blocking the TRAF6-NF-κB pathway.

LYC (lycopene) plays roles in preventing heart disease. Epidemiological studies report that ATR (atrazine)-induced cardiac inflammation is associated with an increase in cardiovascular mortality. However, true confirmation that cardioprotective effects of LYC against ATR-induced heart injury occured through modulation of the inflammation response is lacking. Mice were treated with LYC (5 mg/kg) and/or ATR (50 or 200 mg/kg) by gavage administration for 21 days. These results indicated that LYC significantly protected the heart against ATR-induced histological alterations, including increased NO (nitric oxide) content and NOS (nitric oxide synthase) activities, up-regulation of pro-inflammatory and down-regulation of anti-inflammatory cytokines and activation of the TRAF6-NF-κB pathway. ATR induced cardiac damage via enhancing NO production and triggering the inflammatory response. Supplementary LYC significantly alleviated the cardiac injury via modulating NO and NO-generating systems and blocking the TRAF6-NF-κB pathway. Therefore, LYC showed significant chemoprotective potential against ATR-induced cardiac injury via suppressing the inflammatory response.