Key result
Resveratrol protected cardiomyocytes from cisplatin-induced cardiotoxicity in rats via the suppression of oxidative stress in a dose-dependent manner.
Why the study?
Does resveratrol prevent cisplatin-induced cardiotoxicity in rats?
Does resveratrol prevent cisplatin-induced cardiotoxicity in rats?
Resveratrol demonstrates potential as a cardioprotective agent against cisplatin-induced toxicity without compromising its antineoplastic efficacy in preclinical models.
Does not support clinical use; leaves open translation of resveratrol cardioprotection from rat models to patients.
The clinical use of cisplatin, a potent antineoplastic agent, is limited by its severe adverse effects. The present study was designed to evaluate the effects of resveratrol on cisplatin-induced cardiac injury. Resveratrol is a potent free radical scavenger. In the present study, we tested whether resveratrol would prevent cisplatin-induced cardiotoxicity in rats. Plasma-enzyme activities and histologic myocardial changes were examined. The anticancer role of resveratrol and/or cisplatin were measured by MTT. Our data showed that cisplatin led to cardiac-function deterioration, myocardial injury, increased lactate dehydrogenase, creatine kinase, malondialdehyde activities, and decreased activities of superoxide dismutase, glutathione, glutathione peroxidase, and catalase. Treatment with resveratrol effectively hindered the adverse effects of cisplatin in a dose-dependent manner, such as myocardial injury and impaired heart function. An in vitro cytotoxic study showed that resveratrol could increase the antineoplastic activity of cisplatin to A549 adenocarcinoma cells. All the above lines of evidence suggest that resveratrol protects cardiomyocytes from cisplatin-induced cardiotoxicity via the suppression of oxidative stress.
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Wang et al. (2009) studied Cisplatin-induced cardiotoxicity. Resveratrol vs. Cisplatin alone was evaluated on Cardiac-function deterioration, myocardial injury, and oxidative stress markers. Resveratrol protected cardiomyocytes from cisplatin-induced cardiotoxicity in rats via the suppression of oxidative stress in a dose-dependent manner.
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