Key result
Pretreatment with compound ARL significantly reduced elevated levels of plasma cardiotoxic biomarkers and alleviated doxorubicin-induced depletion of blood glutathione levels in rats.
Why the study?
Does compound ARL prevent doxorubicin-induced cardiotoxicity in female Wistar albino rats?
Does compound ARL prevent doxorubicin-induced cardiotoxicity in female Wistar albino rats?
Compound ARL demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in a rat model by reducing biomarker elevation and oxidative stress.
Should not change doxorubicin use; hypothesis-generating for ARL cardioprotection in humans.
The present study was aimed to evaluate the cardioprotective activity of N-(benzo[d]oxazol-2-yl)-2-(5-bromo-2-oxoindolin-3-ylidene)hydrazinecarboxamide (coded as ARL) in rats. Doxorubicin (DOX) (15 mg kg−1, i.p, single dose) was used to induce cardiotoxicity in rats. Four groups of female Wistar albino rats were used. Group 1 was used as control (0.5% CMC, oral); the other groups were treated with DOX (single i.p. dosage of 15 mg kg−1) or DOX plus compound ARL (50 or 100 mg kg−1 day−1, p.o.), respectively. Animals were treated with ARL or CMC for 7 days. On 6th day, a single dose of DOX was administered to rats. Blood was collected on 7th day. Evaluation of cardioprotective activity was estimated using biochemical parameters including plasma aspartate aminotransferase, creatine kinase (CK-MB), lactate dehydrogenase (LDH), and triglycerides (TG) levels. Pretreatment with compound ARL significantly reduced the elevated levels of cardiotoxic biomarkers in plasma. DOX-induced depletion of glutathione levels in blood was significantly alleviated by pretreatment with compound ARL.
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Reddy et al. (2012) studied Doxorubicin-induced cardiotoxicity. Compound ARL vs. Doxorubicin alone and vehicle control was evaluated on Plasma cardiotoxic biomarkers (AST, CK-MB, LDH, TG) and blood glutathione levels. Pretreatment with compound ARL significantly reduced elevated levels of plasma cardiotoxic biomarkers and alleviated doxorubicin-induced depletion of blood glutathione levels in rats.
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