Circadian clock plays a vital role in the pathological progression of cardiovascular disease (CVD). Our previous studies showed that acrolein, an environmental pollutant, promoted atherosclerosis by reducing CLOCK/BMAL1 and disturbing circadian rhythm. Whereas, intermittent fasting (IF), a diet pattern, was able to ameliorate acrolein-induced atherosclerosis., mice were fed acrolein 3 mg/kg/daydrinking water and IF for 18h (0:00-18:00). We observed that IF decreased acrolein-accelerated the formation of aortic lesion inmice. Up-regulation ofandlevels were found in liver and heart tissue upon acrolein exposure, while was down-regulated by IF. Interestingly, IF treatment exhibited higher AMPK, p-AMPK and SIRT1and lower MAPK expression which was caused by acrolein. Besides, circadian genesexpression were suppressed and disturbed treated with acrolein, while were reversed by IF. Furthermore, consistent with that, short-term starvation as a fasting cell modelcould improve the disorders of CLOCK/BMAL1 and raised SIRT1regulating AMPK, as well as ROS-MAPK induced by acrolein. In conclusion, we demonstrated that IF repressed ROS-MAPK while activated AMPK to elevate the expression of circadian clock genes to ameliorate acrolein-induced atherogenesis, which shed a novel light to prevent cardiovascular diseases. In vivo via ApoE NF-κB, IL-1β TNF-α Clock/ Bmal1in vivo in vitro via -/-
