Key result
Edaravone pretreatment significantly reduced adriamycin-induced cardiotoxicity in rats, decreasing cardiac troponin T levels by 42% compared to adriamycin alone.
Why the study?
Adriamycin is widely used in chemotherapy, but cardiotoxicity limits its clinical use, prompting investigation into whether the potent antioxidant edaravone provides cardioprotection.
Does edaravone prevent adriamycin-induced cardiotoxicity in a rat model?
Does edaravone prevent adriamycin-induced cardiotoxicity in a rat model?
Effect estimate: 42% reduction
Absolute Event Rate: 3560% vs 8288%
p-value: p=<0.001
Edaravone pretreatment significantly attenuated adriamycin-induced cardiotoxicity in rats, as evidenced by improved ECG parameters, reduced cardiac biomarkers, and decreased 99mTc-PYP scintigraphic uptake.
Edaravone may attenuate anthracycline cardiotoxicity; leaves open translation to human trials.
Aim: Adriamycin (ADR) is an antineoplastic drug that is widely used in chemotherapy but its cardiotoxicity is the most important side effect that limits the clinical use of this drug. In this study, we investigated of edaravone (EDO), which is a potent antioxidant, ADR-induced cardiotoxicity model in rats by electrocardiographic (ECG), biochemical and scintigraphic methods. Methods: Twenty-eight adult male Wistar-Albino rats were randomly separated into four groups; namely control (CON); Adriamycin (ADR); substance control of edaravone (EDO), edaravone + adriamycin (EDO+ADR) groups. Cardiotoxicity in rats was induced by adriamycin injection (cumulative dose:18 mg/kg, intraperitoneal-i.p.-) at an interval of 24 hours (h) on the 5 th , 6 th and 7 th days. Rats receiving edaravone treatment in the adriamycin group administration edaravone (30 mg/kg/day, i.p.) for 7 days and were injected with adriamycin (18 mg/kg, i.p.) on 5 th , 6 th and 7 th days. On the 8 th day electrocardiography (ECG), biochemical and technetium-99m pyrophosphate ( 99m Tc-PYP) scintigraphic parameters were assessed. Results: ADR induction caused changes in the ECG pattern, decreased heartbeat, P wave and QRS complex duration, increased both ST-segment amplitude and QT interval duration (p < 0,001), increase in the biochemical markers [blood urea nitrogen (BUN), creatine kinase (CK), cardiac troponin T (cTnT)], and elevated 99m Tc-PYP uptake level (p < 0,001). EDO treatment prevented all the parameters of ADR-induced cardiotoxicity in rats, by significantly decreased all ADR-associated conduction abnormalities in ECG (p < 0.001), decreased 99m Tc-PYP uptake (p < 0.001) and serum BUN, CK and cTnT, (p < 0.001). Conclusions: Our data demonstrate that EDO has cardioprotective effects on DOX-induced cardiotoxicity. At the same time, this study suggested that 99m Tc-PYP may be using as a non-invasive method for the early diagnosis of ADR-induced cardiotoxicity.
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Aygün et al. (2019) studied Adriamycin-induced cardiotoxicity (n=28). Edaravone vs. Adriamycin alone was evaluated on Cardiac troponin T (cTnT) levels (42% reduction, p=<0.001). Edaravone pretreatment significantly reduced adriamycin-induced cardiotoxicity in rats, decreasing cardiac troponin T levels by 42% compared to adriamycin alone.
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