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Protective Effects of 6-Gingerol on Cardiotoxicity Induced by Arsenic Trioxide Through AMPK/SIRT1/PGC-1α Signaling
Xue Han1, Yakun Yang1, Muqing Zhang2
1School of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, China.
Abstract:
Background and Objective: Arsenic trioxide (As2O3) 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 As2O3-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) As2O3 (5 mg/kg); 4) 6G (10 mg/kg) and As2O3 (5 mg/kg); 5) 6G (20 mg/kg) and As2O3 (5 mg/kg). 6G was given orally and As2O3 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, As2O3 was found to induce cardiotoxicity in mice. 6G significantly ameliorated As2O3-induced heart injury, histopathological changes, oxidative stress, myocardial mitochondrial damage, inflammation, and cardiomyocyte apoptosis, while reversed As2O3-induced inhibition of the AMPK/SIRT1/PGC-1α pathway. Conclusion: Our experimental results reveal that 6G effectively counteracts As2O3-induced cardiotoxicity including oxidative stress, inflammation and apoptosis, which might be attributed to its activation action on AMPK/SIRT1/PGC-1α signaling pathway.
Insights
6-Gingerol (6G) protects against arsenic trioxide (As2O3)-induced cardiotoxicity by reducing oxidative stress, inflammation, and apoptosis. This protective effect is linked to the activation of the AMPK/SIRT1/PGC-1α signaling pathway.
Area of Science:
- Pharmacology
- Cardiology
- Natural Products Chemistry
Background:
- Arsenic trioxide (As2O3) is an effective anticancer agent but its clinical use is limited by cardiotoxicity.
- 6-Gingerol (6G), the primary active compound in ginger, possesses numerous health benefits.
- Investigating 6G's protective mechanisms against As2O3-induced heart damage is crucial.
Purpose of the Study:
- To elucidate the pharmacological mechanisms by which 6-Gingerol mitigates arsenic trioxide-induced myocardial injury.
- To evaluate the efficacy of 6G in preventing As2O3-induced cardiotoxicity in a mouse model.
Main Methods:
- A mouse model was established using As2O3 to induce cardiotoxicity.
- Mice were treated with varying doses of 6G or vehicle control.
- Analyses included biochemical assays, histopathology, electron microscopy, ELISA, and Western blotting to assess cardiac function and molecular pathways.
Main Results:
- As2O3 administration led to significant cardiotoxicity, evidenced by histopathological damage, oxidative stress, mitochondrial dysfunction, inflammation, and cardiomyocyte apoptosis.
- 6G treatment markedly ameliorated As2O3-induced cardiac injury and its associated pathological features.
- 6G reversed the As2O3-induced inhibition of the AMPK/SIRT1/PGC-1α signaling pathway.
Conclusions:
- 6-Gingerol effectively counteracts arsenic trioxide-induced cardiotoxicity.
- The protective effects of 6G involve the mitigation of oxidative stress, inflammation, and apoptosis in cardiomyocytes.
- Activation of the AMPK/SIRT1/PGC-1α signaling pathway is a key mechanism underlying 6G's cardioprotective action.
