Key result
Fluvastatin exerted a protective effect against doxorubicin-induced renal and cardiac toxicity in rats by repressing lipid peroxidation and regulating iNOS, eNOS, NF-κB, and Caspase-3 expressions.
Why the study?
Doxorubicin clinical use is limited by severe renal and cardiac toxicities, and fluvastatin has demonstrated antioxidant and anti-inflammatory properties that may offer protection.
Does fluvastatin prevent doxorubicin-induced cardiac and renal toxicity in rats?
Does fluvastatin prevent doxorubicin-induced cardiac and renal toxicity in rats?
Fluvastatin demonstrates protective effects against doxorubicin-induced cardiac and renal toxicity in a rat model by reducing oxidative stress, inflammation, and apoptosis.
Hypothesis-generating for fluvastatin cardioprotection with doxorubicin; animal data only, no practice change warranted.
Doxorubicin (DOXO) is a cytostatic agent used in the chemotherapy protocol of several cancers for more than 40 years, but usage of this drug in cancer treatment has been limited due to severe renal and cardiac tissue toxicities that may result in death in patients. Fluvastatin (FV) is a fully synthetic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor used as a cholesterol-lowering agent in patients with hypercholesterolemia. Previous studies revealed that FV also exhibits antioxidant, anti-inflammatory, and antitumor activity. Additionally, our previous study indicated that FV exerts a prophylactic effect on DOXO-induced testicular toxicity by preventing lipid peroxidation, supporting the antioxidant system, and regulating the blood-testis barrier-associated genes expression. Herein, we purposed to evaluate the possible therapeutic and the protective effects of FV on the DOXO-induced cardiac and renal toxicitiy model by histochemical, immunohistochemical, biochemical, and real-time polymerase chain reaction (real-time PCR) analyses. Results point out protective use of FV exerts a beneficial effect by repressing lipid peroxidation and by regulating the inducible nitric oxide synthase (iNOS), nitric oxide synthase endothelial (eNOS), nuclear factor kappa-B (NF-κB), and Caspase-3 (Casp3) protein and mRNA expressions, which play an important role in mediating DOXO-induced renal and cardiac toxicity mechanisms. In conclusion, FV may be a candidate agent for the prevention of renal and cardiac toxicities in cancer patients receiving DOXO chemotherapy.
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Kuşçu et al. (2022) studied Doxorubicin-induced cardiac and renal toxicity. Fluvastatin vs. Doxorubicin alone (implied) was evaluated on Cardiac and renal toxicity markers (lipid peroxidation, iNOS, eNOS, NF-κB, and Caspase-3 expressions). Fluvastatin exerted a protective effect against doxorubicin-induced renal and cardiac toxicity in rats by repressing lipid peroxidation and regulating iNOS, eNOS, NF-κB, and Caspase-3 expressions.
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