Key result
Ethyl pyruvate treatment significantly improved cardiac function and reduced oxidative stress, fibrosis, and apoptosis in rats with Adriamycin-induced cardiomyopathy.
Why the study?
Does ethyl pyruvate improve cardiac function and reduce oxidative stress, apoptosis, and fibrosis in a rat model of Adriamycin-induced cardiomyopathy?
Does ethyl pyruvate improve cardiac function and reduce oxidative stress, apoptosis, and fibrosis in a rat model of Adriamycin-induced cardiomyopathy?
Ethyl pyruvate attenuates Adriamycin-induced cardiomyopathy in rats by improving cardiac function and reducing oxidative stress, apoptosis, and fibrosis, suggesting potential as a therapeutic agent.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in a rat model; leaves open translation to human Adriamycin cardiomyopathy.
Ethyl pyruvate (EP), a derivative of pyruvic acid, is known to have protective effects against ischemic cardiomyopathy and other disorders. However, little is known about its role in Adriamycin (ADR)-induced cardiomyopathy. The present study was designed to investigate the impact of EP on ADR-induced cardiomyopathy in an animal model. Sixty male Sprague-Dawley (SD) rats were divided into four groups: Normal control, EP, ADR and ADR + EP groups (n=15/group). Rats in the ADR and ADR + EP groups were treated with ADR (2.5 mg/kg/week intraperitoneally) for 6 weeks. From the eighth week, rats in the EP and ADR + EP groups received EP via gastric lavage at a dose of 50 mg/kg/day for 30 days. After completing the EP treatment, cardiac function was assessed by echocardiography and then rats were sacrificed. Hearts were harvested for subsequent analysis. Compared with rats in the normal control and EP groups (without ADR treatment), rats in the ADR and ADR + EP groups showed significant impairments in terms of cardiac function, apoptosis, severe oxidative stress and fibrosis in the heart. However, these impairments were alleviated by EP treatment in the ADR + EP group. Upon EP treatment, cardiac function was significantly improved. The levels of oxidative stress, fibrosis and apoptosis in the myocardial tissues were also significantly reduced. These findings indicated that EP treatment attenuated, at least partially, ADR-induced cardiomyopathy in rats.
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Liu et al. (2016) studied Adriamycin-induced cardiomyopathy (n=60). Ethyl pyruvate vs. Adriamycin alone was evaluated on Cardiac function (fractional shortening and ejection fraction) (p=<0.05). Ethyl pyruvate treatment significantly improved cardiac function and reduced oxidative stress, fibrosis, and apoptosis in rats with Adriamycin-induced cardiomyopathy.
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