Key result
Rosiglitazone treatment in adriamycin-administered rats significantly diminished cardiac dysfunction markers, oxidative stress, and apoptosis compared with adriamycin alone.
Why the study?
The study investigated the effect of rosiglitazone on adriamycin-induced cardiotoxicity in experimental animals.
Does rosiglitazone ameliorate adriamycin-induced cardiotoxicity in adult Wistar male rats?
Does rosiglitazone ameliorate adriamycin-induced cardiotoxicity in adult Wistar male rats?
Answers are grounded in this paper and cite their sources.
Rosiglitazone protects against adriamycin-induced cardiotoxicity in a rat model by reducing oxidative stress and apoptosis.
We investigated the rosiglitazone (RSG) effect on adriamycin (ADM)-induced cardio toxicity in experimental animals. Forty adult Wistar male rats were separated into four groups as follows: normal control; RSG (10 mg/kg)-treated; ADM (10 mg/kg)-administered; and ADM (10 mg/kg) + RSG (10 mg/kg)-treated. Serum lipid level, different biochemical biomarkers, histological analysis, and nuclear factor erythroid 2-related factor/heme oxygenase-1 (Nrf2/HO-1), Caspase 3, B-cell lymphoma 2 (Bcl-2), and Bax gene expression were assessed in serum and cardiac tissue samples. Our results show that RSG treatment in ADM-administered animals significantly diminished low-density lipoprotein cholesterol, triglyceride, and total cholesterol, and increases high-density lipoprotein cholesterol (HDL-c) in comparison with the ADM group. RSG treatment reduced the effect of ADM administration on cardiac dysfunction markers such as cardiac troponin T Creatine Kinase-MB, aspartate aminotransferase, and lactate dehydrogenase, showing the amelioration of cardio toxicity in ADM-administered rats. Additionally, RSG treatment significantly decreased the level of malondialdehyde and nitric oxide in cardiovascular tissue. RSG-treated rats in combination with ADM likewise showed a significant increase in reduced glutathione, superoxide dismutase, catalase content, and the activity of glutathione peroxidase (GPx) as compared with ADM group. Moreover, RSG treatment in ADM rats significantly increased an Nrf2 and HO-1 expression in comparison with ADM group. While in apoptosis parameters, RSG treatment in ADM rats significantly diminished a cleaved caspase-3 and Bax expression as well as expanded Bcl-2 expression when contrasted with ADM group of rats. In conclusion, RSG is capable of protecting heart toxicity in ADM-treated animals through defensive effects on oxidative stress and biochemical markers.
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Zhang et al. (2019) studied Adriamycin-induced cardiotoxicity (n=40). Rosiglitazone vs. Adriamycin alone was evaluated. Rosiglitazone treatment in adriamycin-administered rats significantly diminished cardiac dysfunction markers, oxidative stress, and apoptosis compared with adriamycin alone.
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