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Background and Objective:  Arsenic trioxide (As 2 O 3 ) induced cardiotoxicity to limit the clinical applications of the effective anticancer agent. 6-Gingerol (6G) is the main active ingredient of ginger, a food with many health benefits. The present study aims to investigate the potential pharmacological mechanisms of 6G on As 2 O 3 -induced myocardial injury.   Methods and Results:  Fifty KunMing mice were divided into five groups ( n  = 10) receiving: 1) physiological saline; 2) 6G (20 mg/kg) alone; 3) As 2 O 3  (5 mg/kg); 4) 6G (10 mg/kg) and As 2 O 3  (5 mg/kg); 5) 6G (20 mg/kg) and As 2 O 3  (5 mg/kg). 6G was given orally and As 2 O 3  was given intraperitoneally once per day for seven consecutive days. Biochemical, histopathological, transmission electron microscopy, ELISA, and western blotting analyses were then performed. Based on the resultant data, As 2 O 3  was found to induce cardiotoxicity in mice. 6G significantly ameliorated As 2 O 3 -induced heart injury, histopathological changes, oxidative stress, myocardial mitochondrial damage, inflammation, and cardiomyocyte apoptosis, while reversed As 2 O 3 -induced inhibition of the AMPK/SIRT1/PGC-1α pathway.   Conclusion:  Our experimental results reveal that 6G effectively counteracts As 2 O 3 -induced cardiotoxicity including oxidative stress, inflammation and apoptosis, which might be attributed to its activation action on AMPK/SIRT1/PGC-1α signaling pathway.

Protective Effects of 6-Gingerol on Cardiotoxicity Induced by Arsenic Trioxide Through AMPK/SIRT1/PGC-1α Signaling Pathway